Do your genes make you a criminal?

In the US a murderer is claiming his crime was the tragic consequence of being born a killer. Steve Connor reports on new arguments over whether some people are destined to be bad
STEPHEN "Tony" Mobley has all the attributes of a natural born killer. Nobody could blame his upbringing - he came from an affluent, white, middle-class American family and he was not abused or mistreated as a child. Yet as he grew up he became increasingly violent, and at the age of 25 he walked into a pizza store and casually shot the manager in the neck after robbing the till and joking that he would apply for the job vacancy when the man was dead. That was in 1991. Now Mobley is waiting on Death Row in Georgia to hear whether his appointment with the electric chair is to be confirmed. His last chance of a reprieve rests with a plea from his lawyer that the murder was not the evil result of free will but the tragic consequence of a genetic predisposition. The genes of Tony Mobley, his lawyers argue, meant he was born to kill. The chief witness for the defence is Mobley's aunt, Joyce Childers, who has testified that various members of the Mobley family over the past four generations have inexplicably been very violent, aggressive and criminal, although most of them "mellowed" in middle age. ``There is no legal defence to his crime,'' says Daniel Summer, Mobley's attorney. ``There is only the mitigating factor of his family history. His actions may not have been a product of totally free will." Murder, rape, robbery, suicide, "you name it", the Mobley family has had it, he says. The idea of invoking the Mobley genes as mitigation for the brutal murder of the pizza manager came to Mr Summer after reading about genetics research in the Netherlands. Scientists studying the history of a particular Dutch family had identified a specific genetic mutation that resulted in a chemical imbalance in the brains of some of the males in the family. This, they said, could explain why the same men were prone to unusually violent outbursts. "We applied for $1,000 from the court to see if Mobley had a similar chemical imbalance, but we were refused. However, our appeal to the Supreme Court against the death sentence still rests on his family history of violent behaviour," Mr Summer says. This week, at a closed meeting of scientists at the Ciba Foundation in London, Mobley's family tree will again come under intense scrutiny, this time by researchers studying the link between genes and violence. Deborah Denno, a genetics expert at the law school of Fordham University, New York, will end the conference by saying that it is not a question of whether genetic evidence will ever be admitted to court, but when and under what circumstances.

THERE is nothing new about the notion that criminals are born rather than made; it has cropped up repeatedly over the past century in the continuing debate over nature versus nurture. This is, however, the gateway to a moral minefield. If it could be proved that the criminal urge might be traced to genes, then, some would argue, crime could no longer be blamed on parents, or society, or unemployment, or bad housing, or anything else that is capable of improvement. It would simply be a fact of life for which nobody was to blame, but which would be traceable to a minority of individuals. This has uncomfortable overtones of eugenics, the pseudo-science which held that mankind could be improved by breeding out the bad, and which the Nazis took a step further by their policy of exterminating the Untermenschen. Even if it stopped there, the idea of the "criminal gene" would be controversial enough, but it does not, for modern science opens up new and different possibilities. If there are genes conferring on certain people a genetic predisposition to crime, could they and their carriers be identified, perhaps as early as the womb? What should happen to those embryos? Moreover, if someone is born with a criminal mind, what else should be done with them other than to lock them away for as long as possible? The arguments date back at least to 1870, when Cesare Lombroso, an Italian doctor, devised his theory of the criminal man. The idea came to him in a "flash of inspiration" on a gloomy day in December when he was studying the skull of a notorious brigand: "At the sight of that skull, I seemed to see all of a sudden, lighted up as a vast plain under a flaming sky, the problem of the nature of the criminal - an atavistic being who reproduces in his person the ferocious instincts of primitive humanity and the inferior animals." Enormous jaws, huge eye sockets and handle-shaped ears were the sort of inherent features to be found in "criminals, savages and apes", Lombroso wrote. Throughout the 20th century further attempts have been made to refine what Lombroso started. Many did little to improve on his nonsensical ramblings. As recently as 1968, for instance, scientists thought they had stumbled across another physical marker for criminal behaviour. They found that 3 per cent of the male inmates in a hospital for mentally abnormal offenders had an extra Y chromosome. Enterprising lawyers seized upon this information and used it as defence evidence in court: "My client has the extra Y chromosome; he couldn't help himself." But it was soon discredited when it was shown that the majority of XYY men had no obvious abnormality and were no more likely to be involved in serious crime than normal XY men. The more durable research into the genetics of crime has its roots in 1931, when psychologists began looking at nature's own "experiment" in genetics - twins. Identical twins share exactly the same genes, whereas non-identical twins share about 50 per cent of their genes, just like other brothers and sisters. Comparing the fates of pairs of identical twins and non-identical twins, it was clear, could offer some idea of how much a behavioural trait was due to genes (nature) and how much to upbringing (nurture). Thus the results of twin studies have been at the forefront of the evidence for a genetic component to criminal and antisocial behaviour. Chief of these is the Danish twin study, which has been running for the past quarter- century. Denmark has become a magnet for social psychologists interested in criminal genetics. Not only is it racially homogeneous, with a good health care system (both of which help to standardise data), but every pair of twins born since 1870 has been registered with the authorities, as has every criminal. The Danish twin study has cross-checked criminal records for pairs of identical and non-identical twins to compare their fate. The broad conclusion is that a Danish man with an identical twin who has a criminal record is about 50 per cent more likely to have been in prison himself compared with the average Danish male. Non-identical twins are between 15 and 30 per cent more likely to both have criminal records.

Irving Gottesman, a psychologist at the University of Virginia who has worked on the Danish twin study, believes the results show that "criminals are not born, but the odds at the moment of birth of becoming one are not even". Another Danish study, this time of identical twins who are reared apart in different families, appears to support the notion of being born with a criminal disposition. According to Sarnoff Mednick, a psychologist at the University of California at Santa Barbara, a child whose biological parents are criminals is more likely than other children to begin a criminal career himself even if his adopted parents are law abiding. Yet another Scandinavian adoption study, this time in Sweden, found a link between criminality, genes and alcohol abuse. Michael Bohman, professor of child psychiatry at Umea University, says the results show a clear genetic predisposition to alcohol abuse which leads to a rising tendency towards anti-social or criminal behaviour. "Of course if there was no alcohol in the environment then there would be no alcoholism," he says. "The risk is related to your genes and the amount of alcohol you're swimming in, but not everyone, of course, drowns." Studies on twins and adopted children have always suffered from a basic problem. They can only indicate a possible genetic component to a trait. They cannot find the genes involved, nor can they say much about the mechanisms by which environment or upbringing could overcome the genetic predisposition. Every geneticist knows that even if a trait is 100 per cent genetically determined, that does not necessarily mean that nothing can be done about it. The classic example here is the inherited disease phenylketonuria, which can lead to mental retardation. A simple change in the infant's environment, in this case a diet free of the amino acid phenylalanine, can completely override its genetic "destiny" and the disorder is overcome. The history of studies such as these, especially in relation to the debate over IQ and genetics, is littered with controversy. Conclusions from such work have usually been fiercely challenged and some have had to be withdrawn after other researchers had identified methodological flaws. Today, however, there is a new dimension. ALTHOUGH twin studies go on much as they always have, genetics has become transformed over the past 10 to 15 years. New techniques in molecular biology have enabled scientists to identify specific inherited defects in DNA, the genetic blueprint. One of the most startling pieces of research into the genetics of violence has come out of the Department of Human Genetics at the University Hospital in Nijmegen. This was the work that inspired the unusual plea of mitigation from Tony Mobley's lawyers. The scientists at Nijmegen studied the apparent inherited aggression of the Dutch family. Han Brunner, who led the research team and who will also be attending this week's Ciba conference, has, however, distanced himself from suggestions that he has found a "gene for aggression". "The notion of an `aggression gene' does not make sense," he says, and it would be wrong to suggest that any one gene or collection of genes can account for something as complex as aggressive human behaviour. He emphasises that his research has only demonstrated how a very specific genetic defect can result in a fairly specific behavioural abnormality in one particular family, not society at large. The family spanned four generations and almost a century in time. He found that at various times 14 men in the family had displayed mental retardation combined with unusually aggressive posturing, verbal abuse and sometimes physical violence. There was one instance of rape, two of arson and one of attempted murder. Professor Brunner's investigation soon found that the trait was "sex linked" like the blood disorder haemophilia, which affects only males but is transmitted through the maternal line. Further work identified the gene itself, which is responsible for an enzyme called monoamine oxidase- A.

Defects in the gene of the aggressive men prevent the enzyme from working, so causing a build-up of neuro-transmitters in the brain, perhaps resulting in over-excitation of the nerves in stressful situations. Although this sounded a neat solution to the problem, Professor Brunner was presented with some logical inconsistencies in that drugs blocking monoamine oxidase-A have been used extensively to treat patients with depression, with no apparent increase in violent tendencies. Furthermore, one of the neurotransmitters building up in the men was serotonin, which other researchers have found to depress, rather than increase, the propensity for aggression. Such contradictions serve to reinforce the difficulties of explaining complex emotions in biological terms. Nevertheless, psychologists keep pointing to a clear biological basis for criminal or antisocial behaviour on the basis of their studies on twins and adopted children. Even if there does appear to be a genetic basis to some types of behaviour that lead to criminality, psychologists are almost unanimous in their belief that it does not mean some children are doomed to a life of crime. "Just because it's genetic it doesn't mean to say it's not amenable to environmental intervention," says Judy Silberg, a clinical psychologist at the Virginia Commonwealth University. "If weapons are available and you have kids with, say, attention deficit disorder, it's a set-up. You're setting up a situation to happen." THERE are some bitter opponents of what has become known as "neurogenetic determinism". Steven Rose, a brain researcher at the Open University, is a long-standing critic of those who believe that individual differences in human behaviour, notably IQ, have a genetic rather than environmental basis. He lambastes the "reductionists" who believe there is a raw genetic basis for criminality and violence. The rise in genetic determinism offers no solutions to what are essentially society's problems, he wrote this month in the journal Nature. "Although only the most extreme reductionists would suggest that we should seek the origins of the Bosnian war in deficiencies in serotonin-reuptake mechanisms in Dr Karadzic's brain, and its cure by the mass prescription of Prozac, many of the arguments offered by neurogenetic determinism are not far removed from such extremes." Professor Rose is particularly scathing about a recent attempt by some US researchers to establish a "violence initiative" which would investigate the biological basis of ghetto crime. "As an approach to diminishing the violence of city streets, it would seem unlikely to achieve as significant an impact as would measures to reduce the estimated 280 million handguns currently in personal possession in the United States." This issue excites strong emotions. Two years ago there was public outrage in the US over a federal antiviolence initiative, conceived by Louis Sullivan, a black physician and then secretary of the US department of health and human services. The idea was to help young black people, who are disproportionately involved in violent crime. Part of the initiative involved investigating the ``biological'' basis of violent crime. Civil rights leaders and others became deeply suspicious, especially after one leading scientist cited monkey violence and sexuality as the research rationale. "Maybe it isn't just the careless use of the word when people call certain areas of certain cities `jungles'," he said. Amid uproar, the project was shelved. The notion that crime, genetics and race might be linked has particularly inflamed both proponents and opponents of "genetic determinism". Because skin colour is a genetic trait, because crime statistics show that blacks are more likely to end up in jail than whites, and because an increasing number of researchers appear to believe in a genetic basis of crime and violence, some commentators have jumped to the conclusion that black people are more likely to be involved in crime because of their genes.

The water has been further muddied by the recent publication in the US of a book called The Bell Curve by two right-wing social scientists, Richard Hernstein and Charles Murray. The book argues that IQ has a genetic basis and this accounts for an inherent difference between the IQs of the races. Low IQ people, the book says, are more likely to commit crimes because they lack foresight and cannot understand that robbing someone is wrong. Few, if any, of the psychologists and geneticists at this week's Ciba conference would agree with Hernstein and Murray. They might, however, be persuaded that cold-blooded murderers such as Tony Mobley can have a genetic predisposition to violence and antisocial behaviour which they are born with. The problem for Mobley, and others like him, is that judges and juries may be all too ready to agree and conclude that the only treatment is to lock them up and throw away the key, or, in the case of Mobley, throw the switch on the electric chair.

Criminologists Research Shows Genes Influence Criminal Behavior

Jan. 24, 2012

Dr. J.C. Barnes is an assistant professor of criminology in the School of Economic, Political and Policy Sciences at UT Dallas.
Your genes could be a strong predictor of whether you stray into a life of crime, according to a research paper cowritten by UT Dallas criminologist Dr. J.C. Barnes. Examining the Genetic Underpinnings to Moffitts Developmental Taxonomy: A Behavior Genetic Analysis detailed the studys findings in a recent issue of Criminology. The paper was written with Dr. Kevin M. Beaver from Florida State University and Dr. Brian B. Boutwell at Sam Houston State University. The study focused on whether genes are likely to cause a person to become a life-course persistent offender, which is characterized by antisocial behavior during childhood that can later progress to violent or serious criminal acts later in life.

The framework for the research was based on the developmental taxonomy of anti-social behavior, a theory derived by Dr. Terri Moffitt, who identified three groups, or pathways, found in the population: life-course persistent offenders, adolescent-limited offenders and abstainers. Moffitt suggested that environmental, biological and, perhaps, genetic factors could cause a person to fall into one of the paths.

Genes Show Connection to Crime

UT Dallas criminologist Dr. J.C. Barnes has researched connections between genes and an individuals propensity for crime. Shown is the percentage that genetic factors were found to have influenced whether people became life course persistent offenders, adolescent-limited offenders, or those who never engaged in deviant behaviors, called abstainers.

That was the motivation for this paper. No one had actually considered the possibility that genetic factors could be a strong predictor of which path you end up on, said Barnes, who is an assistant professor of criminology in the School of Economic, Political and Policy Sciences at UT Dallas. In her (Moffitts) theory, she seems to highlight and suggest that genetic factors will play a larger role for the life-course persistent offender pathway as compared to the adolescence-limited pathway.

Adolescent-limited offenders exhibit behaviors such as alcohol and drug use and minor property crime during adolescence. Abstainers represent a smaller number of people who dont engage in any deviant behavior. Barnes and his co-researchers relied on data from 4,000 people drawn from the National Longitudinal Study of Adolescent Health to identify how people fell into each of the three groups. The researchers then compared the information using what is known as the twin methodology, a study design that analyzed to what extent genetic and environmental factors influenced a trait. The overarching conclusions were that genetic influences in life-course persistent offending were larger than environmental influences, he said. For abstainers, it was roughly an equal split: genetic factors played a large role and so too did the environment. For adolescent-limited offenders, the environment appeared to be most important. The analysis doesnt identify the specific genes that underlie the different pathways, which Barnes said would be an interesting area for further research. If were showing that genes have an overwhelming influence on who gets put onto the life-course persistent pathway, then that would suggest we need to know which genes are involved and at the same time, how theyre interacting with the environment so we can tailor interventions, he said. Barnes said there is no gene for criminal behavior. He said crime is a learned behavior. But there are likely to be hundreds, if not thousands, of genes that will incrementally increase your likelihood of being involved in a crime even if it only ratchets that probability by 1 percent, he said. It still is a genetic effect. And its still important. The link between genes and crime is a divisive issue in the criminology discipline, which has primarily focused on environmental and social factors that cause or influence deviant behavior. Honestly, I hope people when they read this, take issue and start to debate it and raise criticisms because that means people are considering it and people are thinking about it, Barnes said.

The idea crime could be in part genetic is extremely controversial because most criminologists argue the root causes of crime are environmental factors such as poverty. But now a group of researchers claims that the genes we are born with could play an even more significant role in our chances of turning to a criminal lifestyle in later years.

A University of Texas study published in the Criminology journal found that although there is no single gene which causes criminal behaviour, there are probably a wide range which play a small part in raising or lowering our chance of offending. Dr J.C. Barnes, one of the co-authors, said: "There are likely to be hundreds, if not thousands, of genes that will incrementally increase your likelihood of being involved in a crime even if it only ratchets that probability by 1 per cent, he said. It still is a genetic effect. And its still important. Researchers looked at three broad groups of people: those who persistently offend throughout their lives, those who only commit crimes in their teens, and those who always obey the law.

They focused on so-called life-course persistent offenders, who are typically guilty of anti-social behaviour during adolescence before progressing to violent or more serious crimes in adult life. Using data on 4,000 people from the National Longitudinal Study of Adolescent Health, the researchers found that while adolescent offenders appeared to be more influenced by the environment, the same was not true of those who became lifelong criminals. The twin methodology used to determine the relative influence of environmental and lifestyle factors did not identify which particular genes were responsible, but suggested what up to 70 per cent of our chance of lifelong criminality could be genetic. Dr Barnes said: "The overarching conclusions were that genetic influences in life-course persistent offending were larger than environmental influences. "For abstainers, it was roughly an equal split: genetic factors played a large role and so too did the environment. For adolescent-limited offenders, the environment appeared to be most important.

AUSTRALIANINSTITUTE OFCRIMINOLOGY trends & issues No. 263 Is There a Genetic Susceptibility to Engage in Criminal Acts? Katherine I. Morley and Wayne D. Hall in crime and criminal justice October 2003 ISSN 0817-8542 ISBN 0 642 53816 6 Australian Institute of Criminology GPO Box 2944 Canberra ACT 2601 Australia Tel: 02 6260 9221 Fax: 02 6260 9201 For a complete list and the full text of the papers in the Trends and Issues in Crime and Criminal Justice series, visit

the AIC web site at: http://www.aic.gov.au Disclaimer: This research paper does not necessarily reflect the policy position of the Australian Government. G enetic theories of the origins of criminal behaviour have been a source of contention for over a century since Lombroso proposed quasi-biological explanations of criminal behaviour (Pick 1989; Andrews 1999). Genetic theories of criminality have been especially controversial within the field of criminology because of the eugenic policies that they inspired that were implemented during the Nazi era (Kevles 1985). The sequencing of the human genome has created a renewed interest in the contribution of genetics to socially disapproved behaviour such as addiction, mental disorders and criminal behaviour. Both the media and the public have shown significant interest in stories relating genes to such disorders and their presumed implications for policy. Criminologists, lawyers and policy makers in the criminal justice field need to be well informed about the results of research on genetics of criminal behaviour and its limitations, a need that will only increase as genetic research on behaviour becomes more sophisticated. There is an understandable fear among criminologists that information on increased genetic risks of engaging in criminal

Toni Makkai Acting Director Debates about criminality have long focussed on the relative contributions of environment and genetics as components of antisocial and destructive behaviour. Although genetic explanations for criminal behaviour have been circulated since the emergence of modern criminology in the 1700s, until recently, there has not been the scientific evidence to substantiate or refute any claims. The past decade or so has seen an increase in research on the genetics of behaviour, including antisocial behaviour. The findings of some of this research have inspired media speculation about its policy implications. Many criminologists are understandably concerned about the potential misuse of this research given the earlier historical experiences with the eugenic use made of biological explanations of crime, and of genetic explanations in particular. This brief paper summarises this evidence. Recent twin studies show persuasive evidence that both genetic and environmental factors contribute to antisocial behaviour. However the genetic evidence indicates that there is no single gene, or even a small number of genes, that predict an increased risk of antisocial behaviour. Where there have been some effects the increase in risk associated with antisocial behaviour is modest.. A technical appendix to this paper discussing candidate genes for antisocial behaviour is available on the AIC website <http:// www.aic.gov.au/publications/tandi2/tandi263.html>.Australian Institute of Criminology 2 acts may adversely affect

strategies used to prevent and deal with people who commit crimes. Some commentators fear that genetic information on criminal predisposition may be used by policy makers to justify reduced funding for programs directed at environmental causes of crime (Wasserman & Wachbroit 2001). More speculatively, there is a concern that the identification of genetic susceptibility to criminality may lead to proposals for genetic screening of the population for susceptibility to criminal behaviour (Rowe 2002). These programmes would aim to identify persons at increased risk of engaging in criminal activities and then intervene in some ways to reduce their risk. Such proposals understandably raise fears of a return to the type of state-sponsored intervention in reproduction, pre-emptive

incarceration or medication, and scientifically sanctioned racism that earlier enthusiasms for biological explanations of crime have prompted (Comings 1996; Andrews 1999; Rowe 2002). Before the policy implications of genetic research are addressed we believe that it is essential to critically examine the current state of research on this topic. Such an examination provides the necessary basis for evaluating the validity and ethical acceptability of speculative proposals for the preventive use of genetic information about individual risks of engaging in criminal behaviour. In this paper we accordingly review current knowledge of genetic influences on criminal behaviour and make some tentative predictions about its future direction. This is a preliminary to a more detailed

analysis. The potential preventive uses of such information by society and the criminal justice system will be the subject of a separate paper. Defining criminal behaviour One of the major challenges in researching the causes of criminal behaviour whether these be genetic or environmental is how we should define it. Criminal behaviour is defined by statute and as such is necessarily a social and legal concept rather than a biological one. In light of this fact, some researchers have argued that criminal behaviours should be examined within the wider context of antisocial behaviour (Rutter et al. 1998). This is the approach we follow in this paper. Three ways of defining antisocial behaviour can be distinguished. The first approach equates it with criminality and

delinquency. Criminality is defined as engaging in activities that result in criminal prosecution or incarceration, while delinquency is defined as engagement in unlawful activities while under the age of 18 (Rhee & Waldman 2002). Information on these types of antisocial behaviour can be collected either through police and court records of criminal offences or via anonymous self-reports of participation in activities that would be considered criminal if they had resulted in arrest and conviction (Rhee & Waldman 2002). This categorisation of criminal behaviours is problematic because it means that what constitutes criminal behaviour is defined by statue and therefore changes over time and varies between countries (Rutter et al. 1998).

The second approach that is often used in genetic studies is to use diagnostic criteria for various personality disorders that are associated with an increased risk of criminal activity, namely, Antisocial Personality Disorder (ASPD). ASPD is characterised by a persistent disregard for, and violation of, the rights of others. It can only be diagnosed in individuals over the age of 18 (First 2000). Three childhood disorders Attention Deficit Hyperactivity Disorder (ADHD), Conduct Disorder (CD) and Oppositional Defiant Disorder (ODD) are also often assessed because they have been identified as risk factors for development of ASPD. ADHD is distinguished by frequent inattention and/or hyperactivity-impulsivity, while individuals with CD display behavioural characteristics that

are comparable to ASPD (violation of societal norms or rules) (First 2000). ODD is similar to CD in that it involves disobedient or hostile behaviour, but if more serious forms of behaviour are present, the diagnosis of CD takes precedence (First 2000). A third approach to antisocial behaviour has been to investigate personality traits that may be risk factors for engaging in criminal behaviour. Aggressiveness and impulsivity have been the most heavily researched traits, usually assessed by personality questionnaires (Rhee & Waldman 2002). Adult hyperactivity, often appearing as ADHD, may also be of interest because individuals who exhibit both antisocial and hyperactive behaviour are more likely to engage in criminal behaviour (Rutter et al. 1998).

These three broad approaches to measurement overlap and are interrelated. For example, a prior diagnosis of CD is part of the criteria for ASPD and approximately half of all children clinically diagnosed with ADHD also have ODD or CD (First 2000). Additionally, childhood aggression has been found to predict adult criminality, and criminality, aggressiveness and impulsivity are also part of the criteria for ASPD (Rhee & Waldman 2002). A number of limitations should be highlighted before considering studies that use these three approaches to investigate the role of genetics in antisocial behaviour. Firstly, these studies are primarily concerned with more serious crimes against property or person. They are not thought to have any significantAustralian Institute of Criminology

3 influence on criminal behaviours such as fraud, embezzlement, or other white collar crimes (Rutter et al. 1998). Secondly, the correlation between these disorders and crime is not perfect. Not all individuals who are diagnosed with ASPD and related disorders will engage in criminal behaviour and not all convicted criminals will meet the criteria for one or more of these disorders (Rhee & Waldman 2002). Finally, most of this research does not aim to identify genetic influences on criminal behaviour per se. Rather these studies aim to find gene variants that increase the risk of developing a particular psychological disorder, which may in turn increase the risk of engaging in criminal behaviour. Heritability and antisocial behaviours

Antisocial behaviour often clusters within families, suggesting that both inherited genetic factors and family environment are risk factors for this behaviour. Twin and adoption studies have been used to separate genetic and environmental influences and to assess the contribution that these factors make to the liability to engage in antisocial behaviour. Adoption studies are those in which individuals with a family history of antisocial behaviour are adopted out to families without such a history. If the majority of adoptees later engage in antisocial behaviour, this suggests that genetic background has more influence on liability than family environment. Twin studies compare the occurrence of the behaviour in monozygotic (MZ) and dizygotic (DZ) twin pairs. If

more MZ than DZ twin pairs both have the disorder, this indicates a genetic contribution to the development of the trait. Statistical models are used to determine the heritability of the trait, that is the contributions made by shared genes as well as the contributions of shared (e.g. family) and non-shared environment. Rhee and Waldman (2002) recently conducted a review of the majority of the twin and adoption studies on antisocial behaviour that have been carried out. They found that although genetic background has a strong influence on whether an individual will engage in antisocial behaviour, the influence of environmental factors is even stronger. These results highlight the fact that even if individuals have a strong

genetic predisposition, they may never engage in any antisocial behaviours if they are not exposed to the necessary environmental factors. Mode of inheritance The manner in which the personality disorders and behavioural traits associated with criminal behaviour are inherited has important implications for research and the potential policy uses of the research. First, all of these behavioural characteristics are determined by many different factors. An individuals risk of developing these disorders or displaying these traits is not determined simply by their genotype; environmental influences such as parenting style, socioeconomic status, and peer groups also play a role (Rutter et al. 1998; Gatzke & Raine 2000). Additionally,

interactions between genetic and environmental factors, and between different genes, probably influence the development of these traits and disorders. Although they have some genetic basis, ASPD and related disorders are not influenced by a single gene, and are not inherited in one of the simple patterns of inheritance identified by Mendel. The consensus view is that these traits are influenced by the additive effects of many different gene variants that are widely distributed throughout the general population rather than confined to a small proportion of individuals. Individuals engage in antisocial behaviour when they inherit a sufficient number of variant genes and are exposed to the right (or wrong) social environment (Comings 2000). Candidate genes

Candidate genes are specific genes that are thought to contribute to an increased risk of engaging in antisocial behaviour. They are usually selected on the basis of information about the brain-related bases of behaviour and personality traits. Association studies are usually used to investigate candidate genes. These studies examine whether one variant of a candidate gene occurs more often in individuals who display antisocial behaviour than in some comparison group. As has been true in studies of many other personality traits, research on candidate genes for antisocial behaviour has primarily focused on genes that influence the ways in which nerve impulses are transmitted and received in the brain. Three such pathways have been investigated in relation to antisocial behaviours.

The serotonergic pathway The serotonergic pathway is involved in brain development and dysfunction in this system is thought to increase aggressiveness and impulsivity (Reif & Lesch 2003). Associations have been found between a number of genes involved in this pathway and antisocial behaviours, namely impulsivity, aggression and ADHD (see Table 1). The dopaminergic pathway The dopaminergic system is involved in reward pathways in the brain (Reif & Lesch 2003). Genes involved in this pathway have primarily been investigated for involvement in ADHD, although one study did find an association with impulsivity and ADHD-related symptoms in violent offenders (see Table 1).Australian Institute of Criminology 4 The noradrenergic pathway

The noradrenergic system functions as a central arousal system (Reif & Lesch 2003). Disruptions to the regulation of the noradrenergic pathway have been implicated in psychological disorders such as anxiety and depression. Only two genes involved in this pathway have been examined for a relationship with antisocial behaviours. They have been found to be associated with ADHD and also impulsivity and hostility (see Table 1). Genes involved in two or more pathways Dopa decarboxylase (DDC) is involved in both the serotonergic and dopaminergic systems. Two studies have provided evidence that suggests the involvement of this gene in ADHD. Monoamine oxidase A (MAOA) is involved in the serotonergic, dopaminergic and

noradrenergic pathways. MAOA has become the focus of much genetic research on criminal or antisocial behaviour because the study by Brunner et al. (1993) identified an association between a mutation in MAOA and impulsive aggression. Although this relationship has not been confirmed outside the family examined in the original study, MAOA has been the focus of a number of studies, some of which suggest that the gene has some influence upon antisocial behaviours. Multi-gene studies The inconclusive results from studies of individual candidate genes for antisocial behaviour reflect the fact that these behaviours are likely to be influenced by the interaction of multiple genes. Each genetic variant that influences antisocial

behaviour will only have only a small impact on an individuals overall predisposition to such behaviour. It is therefore unsurprising that individual studies of single candidate genes do not always produce the same result (Ioannidis et al. 2001). Some researchers have begun to address this problem by studying multiple susceptibility genes for behavioural traits and disorders that increase the risk of engaging in antisocial behaviour. Comings et al. have simultaneously examined multiple candidate genes for their involvement in ADHD, CD and ODD. These studies suggest that some of the genes in the serotonin, dopamine and noradrenergic pathways do influence the development of these disorders (Comings 2000; Comings et al. 2000a; Comings et al. 2000b).

However, some of the results of these studies conflict with the results of some single-gene studies. The authors found that the noradrenergic genes had a stronger influence than other groups, but only single-gene studies of DBH have produced relatively consistent positive results. It remains to be seen whether this inconsistency is due to different research methods, or the fact that the noradrenergic pathway has not been as well investigated in single-gene studies. How much can genes tell us? Genetic research is beginning to identify genetic variants that may have some bearing on an individuals liability to develop antisocial behavioural characteristics. In keeping with the polygenic pattern of inheritance proposed for

antisocial behaviours, the amount that each individual gene contributes to an individuals overall liability is likely to be small. This is evident in Table 1 which summarises the relative risks (RR) and odds ratios (OR) for the candidate genes reviewed above. These measures of risk indicate that an individual with a susceptibility variant of one of these genes will only have ~1.5 times the risk of antisocial behaviour compared to an individual from the general population. Thus an individual will only have a significantly increased risk of engaging in antisocial behaviour if they carry a large number of variant genes. This average RR is consistent with the results of meta-analyses of associations between individual genes and risk of developing a

range of disorders and diseases (Ioannidis 2003). Implications and some tentative predictions This review of genetic research on antisocial behaviour has summarised growing evidence for Table 1: Relative risks, odds ratios and associated behaviours for candidate genes Gene Risk Behaviour Serotonergic system Tryptophan hydroxylase Not available Impulsivity, aggression Serotonin receptors RR=1.24 Impulsivity (males), ADHD Solute carrier family 6, member 4 RR=1.29 ADHD Dopaminergic system Dopamine receptor D4 RR=1.5; OR=1.4 ADHD Dopamine receptor D5 RR=1.57-1.67 ADHD Dopamine receptor D3 Not available Impulsivity, ADHD Solute carrier family 6, member 3 RR=1.2; OR=1.5 ADHD Noradrenergic system Dopamine-beta-hydroxylase RR=1.31 ADHD Alpha adrenergic receptor 2A Not available Impulsivity, hostility Other genes Dopa decarboxylase RR=1.48; 1.63 ADHD Monoamine oxidase A OR=2.8 Impulsivity, aggression, CD, criminal convictionAustralian Institute of Criminology

5 a genetic contribution to antisocial behaviour but it has also indicated that it is highly unlikely that variants of single genes will be found that very substantially increase the risk of engaging in criminal behaviour. Instead, it is much more likely that a large number of genetic variants will be identified that, in the presence of the necessary environmental factors, will increase the likelihood that some individuals develop behavioural traits that will make them more likely to engage in criminal activities. This review has a number of implications for proposed uses of genetic information in crime prevention and offender rehabilitation that we will briefly sketch here and develop in more detail elsewhere. Firstly, adoption and twin

studies of antisocial behaviours suggest that there are significant environmental, as well as genetic, risk factors for these behaviours. Research such as that of Capsi et al. (2002) has also shown that genetic studies are likely to provide information about both types of risk factors. We believe that genetic research is more likely to refine social policies by better specification of environmental risk factors than to divert funds from environmental crime prevention strategies. Secondly, susceptibility alleles for antisocial behaviours only increase risk. They are not deterministic and only poorly predict the likelihood that an individual will engage in such behaviour. Additionally, the presence or absence of environmental risk factors cannot be identified by a genetic test.

Taking this information into account, proposals for populationwide genetic screening for criminality do not appear to be feasible. We believe that eugenic governmental policies such as preemptive incarceration are unethical. Such policies are also impractical because they require genetic tests with high predictive value that do not exist and are unlikely to be found. Thirdly, the majority of genetic research on antisocial behaviours has been conducted on Caucasian populations, and does not aim to identify race-specific susceptibility alleles for antisocial behaviour. The polygenic nature of antisocial behaviour also means that even if a susceptibility allele is found at a high frequency in a particular ethnic group, it is likely that a different susceptibility allele will be found at a similarly high frequency in another ethnic group. We believe it is unlikely

that genetic research in this area will lead to or inspire racist crime policies, but anxieties about this issue need to be addressed by behavioural geneticists. Genetic research on criminal behaviour may, however, have some uses in offender treatment and rehabilitation. Information from genetic studies may be used to develop new treatments for personality disorders such as ASPD, CD, ADHD and ODD that are risk factors for criminal behaviour. Genetic information could also be used to assist in diagnosing offenders who have treatable psychological disorders. Comings et al. (2000b) have suggested that their multi-gene tests could have such diagnostic applications in the future. It is less certain what the consequences of such genetic diagnostic tests may be for criminal cases in which

they may be cited as empirical evidence of a defendants diminished responsibility. Many issues need to be examined in more detail before genetic information could be used in legal settings to assess guilt and to decide upon penalties for criminal acts. An analysis of candidate genes for antisocial behaviours and a glossary is available on the AIC website <http://www.aic.gov. au/publications/tandi2/tandi263. html>. References Andrews, L.B. 1999, Predicting and punishing antisocial acts: how the criminal justice system might use behavioral genetics in Behavioral Genetics: the Clash of Culture and Biology (Eds, Carson, R.A. & Rothstein, M.A.) Johns Hopkins University Press, Baltimore; London, pp. 11655.

Brunner, H.G., Nelen, M., Breakefield, X.O., Ropers, H.H. & van Oost, B.A. 1993, Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A, Science, vol. 262, no.5133, pp. 57880. 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, vol. 297, pp. 85154. Comings, D.E. 1996, Both genes and environment play a role in antisocial behavior, Politics and the Life Sciences, vol. 15, no.1, pp. 846. 2000, The role of genetics in ADHD and Conduct Disorder relevance to the treatment of recidivistic antisocial behavior in The Science, Treatment, and Prevention of Antisocial Behaviours: Application to the Criminal Justice

System (Ed, Fishbein, D.H.) Civic Research Institute, Kingston, NJ, pp. 16-116-25. Comings, D.E., Gade-Andavolu, R., Gonzalez, N., Wu, S., Muhleman, D., Blake, H., Chiu, F., Wang, E., Farwell, K., Darakjy, S., Baker, R., Dietz, G., Saucier, G. & MacMurray, J.P. 2000a, Multivariate analysis of associations of 42 genes in ADHD, ODD and conduct disorder, Clinical Genetics, vol. 58, no.1, pp. 3140. Comings, D.E., Gade-Andavolu, R., Gonzalez, N., Wu, S., Muhleman, D., Blake, H., Dietz, G., Saucier, G. & MacMurray, J.P. 2000b, Comparison of the role of dopamine, serotonin, and noradrenaline genes in ADHD, ODD and conduct disorder: multivariate regression analysis of 20 genes, Clinical Genetics, vol. 57, no.3, pp. 17896.

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