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Licence to kill - The biology of violence
Table of Contents
II. Neuroscientific Context
i. Biological Disorder
ii. Psychological Disorder
Much like the film Gattaca, in which a person's genotype determines their employment, Adrian Raine proposes the use of supposed biological traits to identify and treat potential criminals. In his new book ‘The Anatomy of Violence: The Biological Roots of Crime, published on April 30th 2013, the self-proclaimed neurocriminologist claims that “It’s beyond reasonable doubt that genetic and biological factors contribute to violence”.
The media article “Guilty Knowledge” by Fiona MacDonald, published on July 6th 2013 in the Sydney Morning Herald, reviews the work of Adrian Raine and discusses the ethical and moral considerations behind attempting to identify and prosecute criminals via scientific methodologies.
We chose the article for our project due to the over simplification and sensationalism of the neuroscientific context by the author to rile up a response from the general population. Even though MacDonald is informed by Professor Schofield of Neuroscience Research Australia that it is unlikely that there is a “crime gene”, she continues to attempt to shape public perception by suggesting that whilst it may not be possible now, it is only a matter of time before this changes.
With the recent interest of violent crimes in the media, we will discuss how even though there are biological and psychological factors which can contribute to violent criminal behaviours, there are no specific genes or unique identifiable characteristics of a criminal.
II. Neuroscientific Context
i. Biological Disorder
High Testosterone levels
It has been suggested in the past that high levels of testosterone may predispose someone towards aggressive behaviour and violence, potentially predictive characteristics of a violent criminal. Evidence has been provided showing a correlation between men with high testosterone levels and increased irritability, aggression and assertively to threats (Olweus et al., 1988). Despite this however, contradictory evidence has also been presented. In one such study examining hormonal differences between violent criminals and non-violent men it was concluded that although testosterone levels correlated with hostility, there was no significant difference in testosterone levels between the two groups (Aromaki et al., 1999). Insight into the unclear relationship between testosterone and violent/aggressive behaviour was provided in a study suggesting that basal cortisol levels act to moderate the correlation. This notion lead to the dual hormone hypothesis; that effects of testosterone on social behaviour is moderated by cortisol (Denson et al., 2013).
In considering the underlying effects of cortisol on the aggression-testosterone relationship and that of cortisol’s direct effect on aggression, it has been noted that low cortisol levels have been observed in aggressive subject groups (Yu & Shi, 2009). Research indicates that low basal cortisol levels are required for a positive correlation between testosterone and aggressive behaviour. Furthermore it appears that an imbalance of these two hormones, particularly a high testosterone to cortisol ratio reflects predisposition towards aggression and violence (Montoya et al., 2012).
Cortisol and testosterone are hormones that are both synthesized and secreted in response to higher neuroendocrine systems; the Hypothalamus-pituitary-adrenal (HPA) and the hypothalamus-pituitarygonadal (HPG) axes respectively. These neuroendocrine systems have been linked to passive and aggressive behaviour. A necessary balance is established between the two systems in that the HPA elicits fear potentiation and sensitivity to punishment while the HPG works to establish reward-drive, dominance and aggression. An imbalance between the two systems, reflected through a high testosterone:cortisol ratio may result in an increased frequency of assertive behaviour and decreased withdrawal in the presence of a threat, making a person more likely to respond with aggression when confronted. The pathway through which this is achieved is the dopaminergic mesolimbic reward system, containing within it the amygdala, a structure associated with emotional response and subject to cortisol and testosterone influence (Glenn et al., 2011).
Along with the role of cortisol and testosterone in producing withdrawal or assertive behaviours through the mesolimbic system, these hormones also appear to have a direct effect on the amygdala. There is evidence to suggest that elevated testosterone levels induce vasopressin gene expression within the amygdala and that high levels of vasopressin are associated with aggression (Montoya et al., 2012). In opposition to this effect, high cortisol levels result in enhanced cortotropic release factor gene expression and heightened fear, anxiety and withdrawal behaviour. In addition to influence on gene expression, cortisol and testosterone affect the strength of communication between the amygdala and other brain regions involved in aggression pathways. Increased testosterone has been shown to reduce input and output signals between the amygdala, orbital frontal cortex and other cortical regions resulting in decreased emotional input in decision making and reduced inhibition of assertive impulses and aggressive urges. To conform to the trend, cortisol has an opposite effect on amygdala containing neural circuitry in that it strengthens connections, presumably resulting in more emotional contribution to decisions and judgment as well as enhanced inhibition of dominant behaviour (Glenn et al., 2011).
While there seems to be strong evidence for cortisol and testosterone influence on neural pathways related to aggression it is important to note that this relationship is not yet strongly understood. Androgen testosterone receptors are widespread throughout the brain and spinal cord which supports the likelihood that testosterone might play a role in multiple pathways (Mazur 2013). There is also a suggested role for neurotransmitter influence on hormonal impact on aggression and vice versa. In animal models it has been observed that transgenic mice lacking nitric oxide, a potential neurotransmitter, are highly aggressive and violent until they are deprived of testosterone through castration (Nelson &Trainor 2007). In addition, recent studies have suggested that testosterone and cortisol influence on aggression is mediated by serotonin (5-HT) in that high testosterone levels along with low 5-HT and cortisol levels facilitate aggression (Kuepper et al., 2010).
Due to the wide collection of possible mechanism and controlling factors for testosterone's influence on aggression and violent behavior it is not likely that testosterone is or will come to be a reliable indicator of predisposition towards criminal violence. While there is broad availability of evidence for a testosterone-aggression correlation there also exists evidence that is contradictory. Even the controlling mechanisms such as that of cortisol levels present contradictory evidence in that studies have found high cortisol levels are necessary for a positive testosterone-aggression correlation (Denson et al., 2013). In addition, the validity of evidential studies cannot be indisputably confirmed. It has been argued that due to the confounding effects of social context, pulsatile hormonal secretion and system interconnection a clear picture of testosterone's role in aggression can only be obtained through well devised multi-feature studies. (Mazur 2013; Glenn et al., 2011)
ii. Psychological Disorder
Intermittent Explosive Disorder
There are many psychological disorders of the frontal cortex related to violent/criminal behaviours, however due to co-morbidity it is difficult to specify triggers for the individuals action. Therefore, we will focus on intermittent explosive disorders, a sub-category of the impulse control disorders.
Intermittent explosive disorder (IED) has a lifetime prevalence of 6% in the population, with a higher distribution amongst young males with diagnosis in their early teens. No racial bias has been noted, with the majority of studies being undertaken in the United States and Ukraine (Kessler, 2006). Because of the nature of psychological disorders, diagnosis of IED is difficult and usually happens after other disorders such as antisocial personality disorders, attention deficit hyperactivity disorders, and operation defiant disorders have been ruled out.
Symptoms and diagnosis of IED is defined in the Diagnostics Statistics Manual of Mental Disorders (DSM-V) as:
Several episodes of impulsive behavior that result in serious damage to either persons or property, where in
The degree of the aggressiveness is grossly disproportionate to the circumstances or provocation, and
The episodic violence cannot be better accounted for by another mental or physical medical condition.
It has been suggested that the impulsive violent behaviours associated with IED are correlated with low serotonin turnover rate in the pre-frontal cortex, and has been extensively studies in both animal and human models. (Moul, 2013) If the testing of urine results in a low concentration of 5-Hydroxyindoleacetic acid (5-HIAA), it suggests a reduced level of serotonin turnover, as 5-HIAA is the precursor for serotonin. The reduced levels of serotonin (5-HT) affects the hypothalamus and other vital regions, leading to a disruption of the circadian rhythm and blood glucose regulation. (Virkunnen, 1995) However, due to the nature of the disorder, these symptoms are also common among similar disorders such as Bipolar Disorder. (Kessler, 2006)
Other suggestions include damage to the pre-frontal cortex, specifically the amygdala, which has been linked to an increase in impulsive and aggressive behaviour. As the damage happens to the pre-frontal cortex, IED also correlates to lack of control of the individual’s own actions, and an inability to predict their actions. Likewise with the biological disorder, the lesions have been associated with reduced blood sugar control, leading to decrease in brain function that are associated with planning and decision making.
According to Raine (2013), dysfunction of the prefrontal cortex is one of the hallmark characteristics of a reactive subtype of violent offenders. Raine argues, that among the prefrontal cortex’s many functions is the inhibition of aggressive impulses arising from evolutionary older—and thus presumably more primitive—brain structures, such as those of the limbic system. Consequently, loss of prefrontal control may transform an inconspicuous individual into an impulsive killer, as illustrated by Raine’s account of a man’s rapid descent into violent crime and eventually murder following frontal lobe damage suffered in a car accident (Raine, 2013).
Raine’s claim rests and expands on the widely supported construct of executive functioning, assumed to be implemented by the prefrontal cortex. Executive functioning is said to enable many of the more complex, non-automatic behaviours and abilities seen in humans, such as strategic planning and goal-directed behaviour (Brower & Price, 2001). The prefrontal cortex is thought to support these via a process of top-down biasing—it guides which of those processes competing at any given moment in the brain will find expression in behaviour, by biasing neural activation patterns in their favor (Brower & Price, 2001). This then, would be of fundamental importance should the task-appropriate response compete with a more dominant one. Raine’s view is thus, that executive functioning is necessary for the regulation and inhibition of aggressive impulses.
A classic, well established task to assess executive functioning is the so-called Wisconsin Card Sorting Test (WCST). In 1963, Milner reported that patients with dorsolateral frontal lesions displayed a significant and stereotypical impairment on the WCST. In this neuropsychological test, participants match cards according to different sorting schemes. What scheme applies, the participant has to infer from the researcher’s responses to his matching choices. The sorting scheme changes over the course of the task, forcing the participant to adapt his behaviour. Patients with dorsolateral prefrontal lobe damage typically commit perseverative errors—they appear unable to adapt to a changed sorting system and thus continue sorting to a specific category after it has ceased to be appropriate (Milner, 1963). Surprisingly, the patients are able to verbally express what would be the correct behaviour.
Thus, patients with frontal lobe damage and impaired executive functioning do appear unable to inhibit inappropriate behaviour under some circumstances. However, failing to inhibit a specific—and formerly appropriate—card sorting behaviour seems far less severe an impairment than failing to inhibit the urge to bludgeon someone to death. Beyond the research on the more mundane consequences of reduced executive functioning, is there any evidence that it may cause violent behaviour?
A 2001 review on frontal lobe dysfunction in violent behaviour by Brower & Price concluded, that despite the high correlations between frontal lobe damage and aggressive dyscontrol reported in the retrospective studies under consideration, the actual incidence of violent behaviour seemed “relatively low” (p. 725). No study provided evidence for the claim that prefrontal cortex disorders predict violent crime. Brower & Price (2001) estimated, that clinically significant frontal lobe injury might increase the risk of violence by a mere “10% over the base rate for a given population” (p. 725).
Mood and substance abuse disorders are frequently associated with decreased activity in the prefrontal cortex and common among prison inmates (Brower & Price, 2001; Vicens et al., 2011), and thus need to be controlled for. Unfortunately, many of subjects in the studies under review by Brower & Price (2001) had known or suspected psychiatric disorders, and were thus hardly representative of violent criminals or the population as a whole. Brower & Price thus highlighted the importance of prospective studies with appropriate controls.
Well controlled, prospective studies on the topic still seem to be lacking today. A 2013 article on brain pathology in violent prisoners shows researchers still in anticipation of such studies: “[I]t has to be left to more focused prospective studies to pinpoint circumscribed brain abnormalities that relate to specific psychopathological features that lead to violent crime” (Schiltz, et al., 2013, p. 8). The group’s research demonstrated that brain anomalies are generally elevated in offenders not previously considered to suffer from neurospychological problems. In their sample, prefrontal anomalies were not significantly more prominent than those of any other region (Schiltz et al., 2013).
Overall, well designed, prospective studies are still lacking, and the available evidence for the value of prefrontal cortex dysfunction as a predictor of violent behaviour is weak. Prefrontal dysfunction is therefore certainly not a good enough predictor of violent behaviour to be extensively used in courts.
The target audience can be hypothesized to be the general public with little to no knowledge of Neuroscience, especially as the article was published in the Lifestyle section of the Sydney Morning Herald. The piece was hyper sensationalized, possibly to take advantage of the recent string of violent criminal acts as reported by the media and uses a book with questionable research and credibility as its primary source of information.
However, even though the article feels biased, credible sources such as Professor Peter Schofield are interviewed and furthermore, the article does highlight "Raine is living proof that biology doesn't seal out fate" to suggest that there are two sides to the coin.
Even though genes such as Monoamine oxidase A (MAOA), nicknamed as the warrior gene, had been ruled out as a precursor to violent behaviour in humans (Caspi, 2002), there are biological factors which can trigger violent antisocial behaviour in an individual. Raine, via the article, suggests that triggers such as low-resting heart rate, poor frontal lobe functioning, high testosterone are correlated with violence, and combined with poor social support can lead to criminal behaviours. Whilst we chose to ignore questionable cues such as low-resting heart rate, as we felt this would implicate fit athletes, our research does suggest that there are potential biological links between individuals that demonstrate violent criminal behaviour.
Although it is evident that there are links, we believe that due to the complex nature of these factors, the article and Raine pre-emptively suggest their usage for parole hearing. Further research is needed to help identify and treat these individuals, however it is beyond the scope of this project, and the media article, to discuss the legal and ethical responsibilities of neuroscience in assessing criminals in the judicial system.
Various methods were used to find the sources we used in our wiki. We started out using Google to find broader information on our topic. This is how we chose the main points for the neuroscientific context section. For more in-depth information, Google Scholar was then used to find journal articles, and the UNSW library databases were used if an article was not freely available.
Sources used were generally primary research or literature reviews, and all are peer-reviewed. We aimed to use articles that were published recently, in order to have the most up to date information. However, a few much older articles were also cited as they were relevant for explaining how the widespread belief in physiological causes of violent behaviour originated.
All reviewer comments addressed style and grammatical issues, so we felt this was the most important issue to consider while writing the final version of the wiki. As a result, each member of the group was asked to proofread the wiki at various points while revising it. Another suggestion made by multiple reviewers was that more detail was required. This was easily addressed through doing further research and adding information to each section. The last improvement made was the addition of a header image and diagrams in the neuroscientific context section, to illustrate concepts, present data, and to break up the wall of text and make the page look more presentable.
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Archer, J. (2006). Testosterone and human aggression: an evaluation of the challenge hypothesis. Neuroscience and Biobehavioral Reviews, 30, 319-345.
Brower, M. C., & Price, B. H. (2001). Neuropsychiatry of frontal lobe dysfunction in violent and criminal behaviour: a critical review. Journal of Neurology, Neurosurgery & Psychiatry, 71(6), 720–726. doi:10.1136/jnnp.71.6.720
Denson T.F., Mehta P. H., & Ho Tan D. 2013. Endogenous testosterone and cortisol jointly influence reactive aggression in women. Psychoneuroendocrinology 38(3): 416-424
Glenn A. L., Raine A., Schuq R. A., Gao Y., & Granger D. A. 2011. Increased testosterone to cortisol ratio in psychopathy. Journal of Abnormal Psychology 120(2): 389-399
Kuepper Y., Alexander N., Osinsky R., Mueller E., Schmitz A., & Netter P. 2010. Aggression-interactions of serotonin and testosterone in healthy men and women. Behavioural Brain Research 206(1): 93-100
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Montoya E. R., Terburg D., Bos P. A., & Honk J. 2012. Testosterone, cortisol and serotonin as key regulators of social aggression: A review and theoretical perspective. Motivation and Emotion 36: 65-73
National Institute of Health. (22nd of March, 2013). 5-HIAA.
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Ronald C. Kessler, PhD; Emil F. Coccaro, MD; Maurizio Fava, MD; Savina Jaeger, PhD; Robert Jin, MS; Ellen Walters, MS. (2006). The Prevalence and Correlates of DSM-IV Intermittent Explosive Disorder in the National Comorbidity Survey Replication. Arch Gen Psychiatry, 63, 669-678.
Ronay, R., Galinsky, A.D. (2011). Lex talionis: testosterone and the law of retaliation. Journal of Experimental Social Psychology, 47, 702-705
Schiltz, K., Witzel, J. G., Bausch-Hölterhoff, J., & Bogerts, B. (2013). High prevalence of brain pathology in violent prisoners: a qualitative CT and MRI scan study. European archives of psychiatry and clinical neuroscience, 1–10. Retrieved from
Vicens, E., Tort, V., Dueñas, R. M., Muro, Á., Pérez-Arnau, F., Arroyo, J. M., … Sarda, P. (2011). The prevalence of mental disorders in Spanish prisons. Criminal Behaviour and Mental Health, 21(5), 321–332. doi:10.1002/cbm.815
Virkkunen, M. Goldman, D. Nielsen, D. Linnoila, M. (1995). Low brain serotonin turnover rate (low CSF 5-HIAA) and impulsive violence. Journal of Psychiatry Neuroscience, 20(4), 271-275.
Wang, C., Alexander, G., Berman, N., Salehian, B., Davidson, T., McDonald, V., Steiner, B., Callegari, C., Swerdloff, R.S. (1996). Testosterone replacement therapy improves mood I hypogonadal men—a clinical research center study. Journal of Clinical Endrocrinology and Metabolism, 81, 3578-3583.
Yu Y. Z. & Shi J. X. 2009. Relationship between levels of testosterone and cortisol in saliva and aggressive behaviors of adolescents. Biomedical Environmental Sciences 22(1): 44-49
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