do your genes make you a criminal
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Important Research on criminal mindsTRANSCRIPT
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 badSTEPHEN "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 anti-violence 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.
Criminologist’s 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 co-written by UT Dallas criminologist Dr. J.C. Barnes.
“Examining the Genetic Underpinnings to Moffitt’s Developmental Taxonomy: A Behavior Genetic
Analysis” detailed the study’s 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 individual’s 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
(Moffitt’s) 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 don’t 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 doesn’t identify the specific genes that underlie the different pathways, which Barnes
said would be an interesting area for further research.
“If we’re 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 they’re 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 it’s 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 it’s 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.”
A U S T R A L I A N I N S T I T U T E
O F C R I M I N O L O G Y
t r e n d s
&
i s s u e s
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 individual’s 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 individual’s
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
individual’s 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 individual’s
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 defendant’s
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>.
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