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The biological crime: implications for society and the criminal justice system

INVITED EDITORIAL

The biological crime: implications for society and the criminal justice system

Adrian Raine

Departments of Criminology, Psychiatry, and Psychology, University of Pennsylvania, Philadelphia, USA. E-mail: araine@sas.upenn.edu.

The last 2 decades have witnessed a revolution in our understanding of the criminal mind. For almost a century we have accused poverty, social inequality, and bad neighborhoods as the key culprits in crime causation. These factors almost certainly play a role, but what is new in the 21st century is the increasing recognition that genetic and neurobiological factors are equally important in shaping criminal behavior. The challenges we face in the light of these new findings are multiple, and include how we are going to remediate neurobiological impairments in violent offenders and what are the implications for the newly-emerging subdisciplines of neurolaw and neuroethics.

Genes and crime

There is now little scientific doubt that genes play a significant role in antisocial behavior. Reviews of over 100 twin and adoption analyses provide clear evidence that about 50% of the variance in antisocial behavior is attributable to genetic influences.1 The field is now moving on to the more important, third-generation question of: "Which genes predispose to which kinds of antisocial behavior?" Initial answers are now beginning to be given from molecular genetic studies. If the monoamine oxidase A (MAOA) gene is knocked out of mice, they become highly aggressive, becoming "knock-out" fighters themselves. Knock the gene back in, and they return to their normal behavior patterns. Breakthrough family and community studies of humans have also implicated the MAOA gene in antisocial behavior.2 One meta-analysis shows replicability of this interaction effect.3

The important challenge for this third generation of genetic work on antisocial behavior is to identify not just which genes are associated with antisocial behavior, but also which amongst these genes code for the brain impairments found in antisocial groups. Taking MAOA as an example, this enzyme breaks down serotonin, a neurotransmitter low in antisocial individuals. Males with a common polymorphism (variant) in the MAOA gene have an 8% reduction in the volume of the amygdala, anterior cingulate, and orbitofrontal (ventral prefrontal) cortex.4 These brain structures are involved in emotion and are found to be compromised in antisocial individuals. Consequently, one of the genes linked to antisocial behavior results in structural impairments to brain areas compromised in antisocial individuals - from genes, to brain, to antisocial behavior.

From genes to brain to crime

Yet how does one progress from genes to antisocial behavior? One hypothesis is that gene abnormalities result in structural brain abnormalities which result in emotional / cognitive / behavioral abnormalities which in turn predispose to antisocial behavior. There is increasing evidence for brain impairments in antisocial groups, with particularly strong evidence for the prefrontal cortex.5 Neurological patients suffering damage to the ventral prefrontal cortex exhibit psychopathic-like, disinhibited behavior, autonomic and emotional blunting, and bad decision-making.6 Magnetic resonance imaging (MRI) research has shown that those with antisocial personality disorder have an 11% reduction in prefrontal gray matter, together with reduced autonomic activity during a social stressor eliciting "secondary" emotions of shame, embarrassment, and guilt.7 The antisocial individuals with the least amount of gray matter also showed the least autonomic stress responsivity. Different clinical neuroscience paradigms are beginning to converge on the same conclusion that there is a significant brain basis to antisocial behavior, and that these neurobehavioral processes are relevant to understanding violence in everyday society.

Structural prefrontal impairments are paralleled by functional prefrontal impairments (i.e. reduced brain functioning) in a wide range of antisocial populations. Murderers have been found to show reduced glucose metabolism in the prefrontal cortex.8 This impairment also specifically characterizes impulsively violent offenders, suggesting that the prefrontal cortex acts as an "emergency brake" on runaway emotions generated by limbic structures. Brain imaging studies are supported by findings from neuropsychological, neurological, and psychophysiological studies, indicating robustness of findings.

Are these brain impairments caused by environmental factors or by genes? A significant role of genetics is hypothesized to operate for two reasons. First, the structural prefrontal impairment found in antisocial individuals was not accounted for by environmental risk factors for antisocial behavior (e.g. history of head injury, child abuse) or by drug/alcohol abuse.7 Second, an elegant methodological marriage of structural brain imaging with the behavioral genetic twin design demonstrated that genes explain 90% of the variation in the volume of prefrontal gray matter in humans.9 These two arguments, taken together, would strongly suggest that the structural impairments in antisocials have a significant genetic basis, although future studies could still identify some role for the environment.

The role of the social environment

Although genes are likely implicated in the cause of crime, psychosocial processes cannot be ruled out and could be critical. Environmental influences early in development could directly change gene expression, in turn altering brain functioning and resulting in antisocial behavior. Early environmental influences can alter gene expression which then gives rise to the cascade of brain-behavior events outlined above. The exciting concept is that although 50% of the variance in antisocial behavior is genetic in origin, genes are not fixed, static, and immutable; psychosocial influences can result in structural modifications to DNA that have profound influences on neuronal functioning, and hence antisocial behavioral outcome.

Social environment can interact with genetics and biological risk factors for antisocial behavior in other ways.10 Criminal and violent behavior is exponentially increased when social and biological risk factors combine. Studies from several countries have shown that birth complications (including anoxia, known to particularly damage the hippocampus) interact with negative home environments (e.g. early maternal rejection of the child) in predisposing to adult violent offending. There is also replicated evidence that an abnormality in the MAOA gene interacts with early child abuse in predisposing to adult antisocial behavior.2

Social processes can also moderate the biology - antisocial relationship. Reduced prefrontal glucose metabolism particularly predisposes to violence in those from benign home backgrounds. Low physiological arousal is particularly associated with antisocial behavior in individuals from benign home backgrounds. In these cases, where the individual lacks social risk factors that "push" them towards antisocial behavior, biological factors have a greater explanatory role.10 In contrast, the link between antisocial behavior and biological risk factors in those from negative home environments may be weaker because social causes of crime "camouflage" the biological contribution.

Treatment implications

Biology is not destiny and it should ultimately be possible to remediate neurobiological risk factors. The fundamental question is: "If criminals have broken brains, can they be fixed?" Ultimate solutions could be both natural and surprisingly simple. Poor nutrition in the first 3 years of life has been associated with long-term antisocial behavior throughout childhood and late adolescence.11 Controlling for intelligence quotient (IQ) abolishes this relationship, supporting the model that poor nutrition leads to poor brain functioning, resulting in neurocognitive impairments that predispose to antisocial behavior. Fish oil is rich in omega-3, a long-chain fatty acid making up 40% of cell membrane, and dietary supplementation has been associated both with increased IQ, and reduced serious antisocial behavior in prisoners.12 Prevention programs that manipulate nutrition early in life have resulted in reduced delinquency13 and criminality.14 Environmental manipulations can in theory reverse brain risk factors for crime.

An alternative approach is to remediate the neurotransmitter abnormalities produced by gene abnormalities. Serotonin-related genes regulating serotonin's transportation back to the cell body from the synaptic cleft have recently been linked to antisocial-aggressive behavior in children and adults. Given that antisocial-aggressive individuals have low serotonin, medications which increase the availability of serotonin such as Prozac (a selective serotonin reuptake inhibitor) ought to lower antisocial behavior if there is a causal connection. There is evidence to support this prediction in both aggressive adults and children.15

Neuroethical and neurolegal implications

Despite this positive evidence, the fact remains that society is reluctant to use medication to treat aggressive and criminal behavior, while at the same time being comfortable in medicating other behavioral conditions. Paradoxically, because the environment influences gene expression, our neurobiological make-up is ever-changing, whether we like it or not. Should society move towards grasping the biological nettle in order to snuff out crime and violence and reduce suffering? Or should it instead turn a blind eye to new clinical neuroscience knowledge and prohibit tampering with humankind's biological essence, even if this results in lives being lost which could have been saved by biological prevention efforts?

An additional neuroethical concern is that of responsibility and punishment. If a murderer suffers brain impairments predisposing him to commit impulsive violence, are we to hold him/her fully accountable for their behavior? Groundbreaking research is elucidating the neural mechanism that subserves moral decision-making.16-18 From a moral judgment standpoint, given the evidence that the neural circuits underlying moral feeling and decision-making are impaired in antisocial populations,5 are such individuals as capable as the rest of us in knowing - and doing - what is right? A psychopath may know the legal difference between right and wrong, but do they have the feeling of what is right and wrong? Emotions are believed to be central to moral judgment, and they provide the driving force to act morally. In this context, how moral is it for us to punish many criminals as harshly as we do? On the other hand, are there not significant dangers in loosening our concept of accountability? The very concept of "from genes to brain to antisocial behavior" raises neuroethical questions that need to be aired in order for prevention science to progress.

A new generation of clinical neuroscience research that encapsulates brain imaging and molecular genetics is giving rise to the concept that specific genes result in structural and functional brain impairments that predispose to antisocial, violent, and psychopathic behavior. A critical next step in testing the "from genes to brain to antisocial behavior" hypothesis is to conduct molecular genetic and brain imaging research on the same population in order to identify the genes coding for both brain structure/function abnormalities and antisocial behavior. The next empirical step is to ascertain whether antisocial, psychopathic individuals evidence abnormal processing of moral dilemmas. How we will deal with this new knowledge at societal and legal levels is a significant neuroethical challenge concerns. The more we learn about the neurobiological causes of crime, the more difficult questions arise concerning culpability, punishment, and freedom of will. The future scientific and neuroethical challenges for the emerging field of neurocriminology can best be met by integrative cross-disciplinary research that bridges traditional macrosocial theories (emphasizing broad social constructs) with new perspectives from clinical and social neuroscience to better understand, and ultimately prevent, antisocial behavior children and crime in adults.

References

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Publication Dates

  • Publication in this collection
    01 Dec 2008
  • Date of issue
    Apr 2008
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