Biological Factors in Crime
Updated: 7 December 2016
Are criminals born or ‘made’? This is a question which has vexed philosophers for millennia and psychologists and sociologists since the dawn of the behavioural sciences early in the 19th Century. The deterministic view offered by biological explanations for criminality – ie: you have no real choice, it’s in your biological make-up – have major implications for how society treats criminals – especially violent ones. Biological theories assert criminal behaviour has a physiological origin, with the implication that the ‘criminal’, therefore, has difficulty not committing crime because it is ‘natural’ – ie: the ‘born criminal’ concept.
Biological determinism can be used to undermine the legal concept of criminal responsibility: criminals are held to be personally and morally accountable for their actions. Only when the Law of Diminished Responsibility is applied in cases of self-defence and mental illness – and in some countries (eg: France) ‘crimes of passion’ (temporary insanity) – is the defendant assumed not to have acted from their own free will.
3 cases illustrate how biological arguments have been used as mitigating factors to reduce the level of criminal responsibility:-
- In 1994 Stephen Mobley was sentenced to death for shooting dead the manager of an American branch of Domino’s Pizza. He was also found guilty of other violent offences, including assault and armed robbery.
While he was on ‘death row’, his legal team searched his family history and found that four generations of his family – including uncles, aunts and grandparents – had committed a range of violent and criminal acts, including rape and murder. His lawyers argued on appeal that Mobley must have inherited a ‘criminal gene’ and, therefore, could not be held responsible for his actions. On this occasion the judge rejected the argument and confirmed Mobley’s death sentence. (Maia Szalavitz, 2012)
- In Italy in 2007 Abdelmalek Bayout was given a 9-year sentence after he admitted to stabbing and killing a man. His sentence was reduced by a year after the judge learned he had a mutated gene linked to aggression. (Ewen Callaway, 2009)
- In the US in 2010 Bradley Waldroup escaped a conviction for first-degree murder (of his wife). Following the presentation of evidence that he possessed the so-called ‘warrior gene’ and had been abused as a child, the jury could only find him guilty of voluntary manslaughter (Nigel Barber, 2010).
As the Waldroup case illustrates, there is often an interaction between environmental experiences and the individual’s biology which may lead to violent and criminal behaviour – effectively epigenetic modification. Biological theories tend to ignore such environmental and psychological factors though they may equally may play a role in explaining such behaviour. Therefore, it is better to think of ‘biological factors’ rather than theories in explaining crime.
Early Biological theories
Many Biological theories are concerned with the concepts of Genetics.
The main thrust in Genetics is that certain characteristics and dispositions are carried on alleles (variations) of genes and, thus, are heritable through reproduction.
The first real modern Biological theory of crime was that of Italian army doctor Cesare Lombroso (1876) who considered criminals to be evolutionarily backward. Based on the physical measurements he collected from Italian prisoners and non-criminal military personnel, Lombroso held that many criminals had been born with ‘atavistic’ features. Criminals had definite biological failings that prevented them from developing to a fully human level. They showed certain ape-like characteristics or sometimes just ‘savage’ features. Such physical anomalies included facial assymmetry, low sloping foreheads, large jaws, high cheek bones, large ears, long arms, thick skulls, dark skin and extra nipples, toes and fingers. In his original theory, possessing 5 or more such qualities inevitably led to a criminal type. Thus, particular types of criminals could be identified by the presence of certain features. Eg:-
- murderers have thin lips, bloodshot eyes, curly hair and long ears
- robbers have beak-like noses
- fraudsters have thin and weedy lips
- sexual deviants have glinting eyes. swollen fleshy lips and projecting ears
According to Lombroso, such people are often insensitive to pain and prefer forms of behaviour that are normal among apes and savages but criminal in human societies. They will frequently indulge in other degenerate behaviour such as having tattoos(!) and participating in orgies.
While Lombroso claimed to be methodical and scientific in the way he conducted his research – examining the skulls of 383 dead criminals and 3839 living ones – his research was flawed in that his sample group included a number of individuals with severe learning difficulties. Furthermore, he appears not to have considered that poverty could be the cause of some of his subjects’ appearances rather than genetics. Nor does Lombroso appear to have considered the role of the social reaction to a child being ‘unattractive’. Research has shown consistently that ‘attractive’ people tend to do better in life than unattractive people – see: Attractiveness Factor. Therefore, an unattractive child, rejected and stereotyped for their looks, is more likely to become marginalised and turn to crime for acceptance in a delinquent sub-culture. (See: SocioPsychological Factors in Crime.) Interestingly, though, Richard Kurtzberg et al (1978) found that offenders in the USA, given facial cosmetic surgery, tended to do better on release from prison than those who had not had the surgery,
Initially Lombroso claimed all criminals were born, not made. Later he modified his theory somewhat, claiming about 40% of all criminals were ‘born criminals’ of this kind, driven into criminality by their biology. Making some acknowledgement of other factors, he allowed that other law-breakers were simply occasional, circumstantial offenders and did not have the atavistic characteristics of the born criminal.
Charles Goring (1913) made an extensive study of 3,000 English convicts and 3,000 non-convicts but could not find the distinctive peculiarities identified by Lombroso. However, he did find a common factor of low intelligence among the prisoners.
He attributed this to genetics – in this respect at least, his study supported Lombroso’s assertion that criminals are born not made.
While Lombroso’s ideas were often ridiculed during the second half of the 20th Century and much made of his poor sampling methods (often using mentally-disturbed and retarded individuals) and flaws in his methodology (eg: no control groups), David Garland (1994) asserts that much of what we today think of as ‘criminology’ got its start with Lombroso who attempted to give criminology scientific credibility, in which the objective measurement and categorisation of the criminal classes could be conducted. (Prior to Lombroso, crime and criminal behaviour were the preserve of religious and philosophical debate.)
Another key Biological theory was that of William Sheldon (1942) who argued that an individual’s body shape (somatype) was correlated with their personality. From a study of more than 4,000 photos of student male physiques and 650 possible personality traits, Sheldon differentiated 3 main somatypes:-
- Ectomorph (thin, wiry frame) – introverted and restrained
- Endomorph (heavy and rounded) – sociable and relaxed
- Mesomorph (solid, muscular frame) – aggressive and adventurous
The extent of each was based on a 7-point scale, with most males being a mix of each type.
From a sample of males in a rehabilitation centre, Sheldon identified a significant proportion as mesomorphs. Sheldon Glueck & Eleanor Glueck (1950), working with 500 males from different offender populations, had similar findings.
One explanation for this is that the mesomorph is more likely to get involved in crime at an early age due to his intimidating appearance. However, a counter argument is that the prisoners’ more muscular bodies may have developed from the hard manual labour as part of the prisons’ work regimes. Philip Feldman (1977) talks of a ‘selection effect’ in which certain people, because of characteristics such as their build, are more likely to be recruited into criminal activity. There is also the labelling effect to be considered – that the police are more likely to suspect certain people of having been involved in an incident because they stereotype people with that build as more likely to be ‘criminal’. The more the police arrest and interrogate people with that kind build, the more likely to find criminals among them. (A kind of self-fulfilling prophecy!)
Michael Wadsworth (1979) found that those in the UK who commit more serious offences are generally smaller in physique and reach puberty later than non-delinquents. However, in their famous longitudinal study of London working-class males, Donald West & David Farrington (1973) – see: Cambridge Study in Delinquent Development – found no association between delinquency and body shape. Curt Bartol (1999) cautiously advises that mesomorphy may be related to teenage offences but not to adult ones.
As to whether there is a genetic element in criminality, Johannes Lange’s classic 1931 study of monozygotic (MZ) and dizygotic (DZ) twins is instructional. 13 pairs of MZ twins and 17 DZ pairs were studied with regard to a variety of ‘criminal indicators’, such as having a criminal record. The MZ twins had a concordance rate of 77% compared to just 12% of the DZ twins. This suggests very much that there is a genetic element in criminality. However, the sample sizes were rather small. A study by Michael Lyons et al (1995) looked at misbehaviour and juvenile crime in thousands of twins; there was little difference between the MZ and DZ twins in early criminal behaviour. However, they did find more similarity in MZ adult twins for criminal and aggressive behaviour. This maturational effect could be due to environmental factors being controlled more (by parents) when they were children. Peter McGuffin & Irving I Gottesman (1985) found concordance rates of 87% for DZs involved in aggressive and anti-social behaviour. Such findings suggest the environment may be as, if not more, important than genetics in determining criminal behaviour. Such a conclusion appears to be contradicted by Karl Christiansen (1977) who looked at 3,586 twin pairs in Denmark and found a 52% concordance rate for criminality in the MZ twins and 22% for DZs. While Christiansen’s work is open to criticism – not least because the correlation was for property crimes, not other crimes – generally records of criminal and aggressive behaviour in adult twins show higher concordance rates for MZs.
Bartol reckons the average concordance rate for MZ twins is 55%, compared to 17% for DZs. Robert Plomin (2001) argues that even identical twins are treated differently by their parents and, therefore, environmental factors can confound assumptions about MZ concordance rates. He argues that MZ twins are only 40% similar in criminality due to genes.
Emil Coccaro et al (1997) focused purely on aggressive behaviour, rather than more general criminal or anti-social behaviour. From 182 MZ twin pairs and 118 DZ twin pairs – all male – they concluded that genes accounted for more than 40% of individual differences in aggression. However, they also concluded that environmental influences accounted for around 50% of individual differences in physical aggression and about 70% in verbal aggression.
There are a limited number of studies looking at adoption of children from parents with criminal records. Fini Shulsinger (1972) studied 57 adopted adults in Denmark who were psychopathic and found that 3.9% of the biological relatives could be classified as psychopathic. This compared to only 1.4% of the relatives of the non-psychopathic adopted control group. However, the figures are small, not statistically significant and Shulsinger’s definition of Psychopathy – impulse-ridden behaviour – as been criticised as too loose. Sarnoff Mednick, William Gabrielli & Barry Hutchings (1987) took all the court convictions between 1927 and 1947 in Denmark and found over 14,000 by adoptees. The researchers then investigated the biological parents of these people for criminal convictions and found a very strong relationship between persistent offenders, particularly male, and having a biological parent convicted of a crime. The table left shows the percentage of sons who have criminal records and whether the biological and adoptive parents also have a criminal record. The correlation with having just a biological parent with a criminal record is almost as strong as having both a biological and an adoptive parent with criminal records. Michael Bowman (1996) found some similar patterns in Sweden – also shown in the table left – from examining 913 women and 862 men from the Stockholm Adoption Study. While the sample sizes of these studies are impressive – especially Mednick, Gabrielli & Hutchings – they are it is still vulnerable to accusations of cultural bias as the sample came from just one small part of Europe.
Mednick, Gabrielli & Hutchings also found there was no relationship in the types of crime committed and that improvements in social conditions tended to reduce crime, indicating a substantial environmental effect. A little earlier in Denmark Katherin Van Dusen et al (1983) found the influence of biological criminal parents was greatest for lower social classes and males, and for property offences only.
Dehryl Mason & Paul Frick (1994) meta-analysed 12 twin and 3 adoption studies investigating the genetics of criminality – overall providing a sample group of 3,795 twin pairs. From this, they estimated that nearly half (48%) of the variation in anti-social behaviour in the general population is genetically controlled. They also estimated greater genetic influence for more violent behaviours than for less violent behaviours. Mason & Frick’s findings were in contrast to the findings of a meta-analysis of 38 studies of twins, families and adoptions by Glenn Walters (1992) who concluded that, while genetics played a part in the development of criminality, it was only a small part. (Walters also concluded that the methodology of pre-1975 studies was poor enough to make them unreliable.) Other problems in adoption studies include the amount of time spent with the biological parents before adoption – the ‘contamination effect’ – and the fact that adoption agencies tend to select adoptive families similar to the biological ones. The findings from Donna Miles & Gregory Carey’s (1997) meta-analysis of 24 twin and adoption studies were more in support of Mason & Frick, finding genetic influence accounted for as much of 50% variance in aggression. They also found that environmental/family influences lessened and genetic influence increased as people got older. Again, this could be an epigenetic effect. However, Soo Rhee & Irwin Waldman’s (2002) meta-analysis lessened the genetic influence to 40%, with environmental influences accounting for 60%. Covering 57 twin and adoption studies, with a total of over 87,000 individuals, this is an impressive study in many ways – with ‘anti-social behaviour’ operationalised as psychiatric diagnoses like Anti-Social Personality Disorder or delinquency or behavioural aggression. Importantly, from a methodology point of view, Rhee & Waldman distinguish between self-reporting of aggression studies (39% genetic component) and assessment by another person (53%), suggesting strongly that the method of assessing aggression moderates the results. Also taking into account the definition of aggression and the age of those under study, Rhee & Waldman found that the genetic contribution could vary from 0% to 75%.
In summary, there does seem to be a genetic influence in criminality but studies are contradictory (and sometimes confusing!) as to the strength of that genetic influence.
The differing results of studies into the relationship between genetics and criminality – some (eg: Christiansen) appearing to show a substantial genetic influence while others (eg: McGuffin & Gottesman) indicating much greater environmental influence – may be explained by the concepts of Epigenetics. As the influence of genes is regulated through various environmental stimuli, it may be that genetic potentiality for ‘criminal behaviour’ is inhibited in some by their experiences and facilitated into development in others via different environmental experiences.
Genes and neurotransmitters
Wolfgang Retz et al (2004) looked at the relationship between violent behaviour and the variant gene 5-HTTLPR in 153 men attending psychiatric assessments with respect to criminal behaviour. The researchers found an association between a particular form of the gene and violent behaviour when the individuals had ADHD as children but not when they had symptoms of personality disorder or impulsivity. Retz et al concluded that the 5-HTTLPR gene, which controls aspects of the neurotransmitter serotonin, is associated with violent behaviour in male criminals. Interestingly Matti Virkkunen et al (1987) found that impulsively-violent offenders had a lower than average serotonin turnover (measured by levels of serotonin in their cerebrospinal fluid). According to Matti Virkkunen et al (1989), they are also more likely to commit further violent crimes after being released from prison. Gerald Brown et al (1982) found that the major metabolite of serotonin tends to be low in the cerebrospinal fluid of people who exhibit impulsive or aggressive behaviour. Historically tryptophan, a serotonin precursor, has been given to juvenile delinquents and unpredictable institutionalised patients to reduce aggressive tendencies, leading Richard Davidson, Katherine Putnam & Christine Larson (2000) to suggest that serotonin may have an inhibitory function. They propose that individuals prone to violence and aggression have serotonergic projections into the prefrontal cortex that are faulty. Experimental evidence to support this comes from Luca Passamonti et al (2012) who showed angry, sad and neutral expressions to participants whose diet was manipulated to be tryptophan-normal or tryptophan-depleted on consecutive days. On tryptophan-depleted days, fMRI scanning showed weaker communication between the prefrontal cortex and the limbic system while the participants reported feeling more aggressive. This study suggests that lower serotonin levels (due to depleted tryptophan) made it more difficult for the prefrontal cortex to regulate the emotional responses generated by the limbic structures.
The connection between lowered serotonin levels and aggression has been reported by Anne Moir & David Jessel (1995), citing a number of animal studies. The link was demonstrated experimentally in humans by John Mann, Victoria Arango & Mark Underwood (1990) who administered the drug dexfenfluramine to 33 adult males and found that males, but not females, reported greater feelings of hostility and aggression on a post-administration questionnaire. The drug, developed to help with weight loss but now withdrawn, is known to deplete serotonin levels in the brain. The gender difference reported by Mann, Arango & Underwood was also found by Terrie Moffitt et al in 1998. Moffitt et al carried out a large-scale study of 781 men and women aged 21, using both self-reporting and court convictions. However, Moffitt et al pointed out that their findings were only correlational and not causal. Olivier Cases et al (1995) demonstrated, from mice studies, that serotonin, especially in the prefrontal cortex, has a calming, inhibitory effect on neuronal firing while Markku Linnoila & Matti Virkkunen (1992) concluded that low levels of serotonin are linked to “impulsivity and explosive acts of violence”. However, it may not be the lack of serotonin itself which is the key factor but, rather, the consequent increase in the density of serotonin receptors. Serotonin receptor density has an inverse relation to levels of serotonin in the brain. Thus, there will likely be an increase in the number of receptors when there is chronic serotonin depletion. Evidence of the effects of increased serotonin receptor density comes from Ramesh Arora & Herbert Meltzer’s (1989) study which found a relationship between violent suicide and elevated serotonin receptor density in the frontal cortex. Similarly, Mann, Underwood & Arango (1996) found that, among suicide ‘completers’, those with increased numbers of prefrontal cortex serotonin receptors had chosen more violent methods of suicide.
The negative correlation of low serotonin/greater aggression is supported by the 2013 meta-analysis conducted by Aaron Duke et al who found a correlation coefficient of -0.12 – small but statistically significant, with their review covering 175 studies and a participant total of around 6,500. (Duke does warn, however, of methodological issues in some of the studies reviewed.)
Seemingly-contradictory results were obtained by Hans Brunner et al (1993) in their study of 5 male members of a Dutch family from Nijmegen who all demonstrated borderline mental retardation and abnormal aggressive behaviour, including violence, arson, attempted rape and exhibitionism. (One man had tried to rape his sister and tried to stab the warden of a mental hospital with a pitchfork; another had tried to run his boss down with a car!) One member of the family had traced this ‘condition’ back to 1870, identifying 9 other males who demonstrated similar behaviour. Data was collected from analysis of 28 family members’ urine samples over a 24-hour period. They found the aggressive behaviour was linked to a point mutation of the gene for monoamine oxidase type-A (MAO-A), the enzyme which breaks down serotonin (and dopamine and noradrenaline), on the X chromosome. Since the mutation was associated with a lack of this enzyme, it would be more difficult for the body to dispose of serotonin. Brunner et al found excess levels of serotonin (and dopamine and noradrenaline) in the men’s urine and concluded that the lack of MAO-A led to poor serotonin metabolism which was linked to the mental retardation which in turn predicated violent behaviour. However, not all the men in the family were violent, even when they were mentally retarded. The sample size, of course, was very small! Brunner did not attempt to claim that the gene responsible for MAO-A is the gene for aggressive behaviour, merely that a genetic deficiency may influence behaviour.
The same point mutation has been found since in 2 other families (Amélie Piton, Claire Redin & Jean-Louis Mandel, 2013) and the condition is sometimes referred to as ‘Brunner Syndrome’.
A marginally-less potent variation (allele) of the gene Brunner et al identified – termed MAO-A-L because it leads to a lower level of the MAO-A enzyme – has been popularised as the ‘warrior gene’ by the likes of Ann Gibbons (2004) and Rose McDermott et al (2009). Studies such as those by McDermott et al and Andreas Meyer-Lindenberg et al (2006) have found a low but significant correlation between MAO-A-L and a tendency to aggression and violence. It should be noted that McDermott et al’s study required some form of provocation for violence to ensue. This tendency, it seems, can be exacerbated through certain negative experiences such as being abused as a child (Peter Crampton & Chris Parkin, 2007; Giovanni Frazzetto et al, 2007) – an epigenetic effect.
There is some evidence that certain racial/ethnic groups may have a greater incidence of MAO-A-L than others. Eg: Rod Lea & Geoffrey Chambers (2007) asserted that only 34% of the Caucasian men in their sample carried the MAO-A-L variant whereas 54% of Chinese men did, 56% of Maori men and 59% of Afro-Caribbean men. Almost inevitably such studies have proved highly contentious, provoking heated debate. Such a reaction can easily be presented as the GREEN vMEME trying to enforce the meme of political correctness that all races and ethnic groups are equal, with one not being inferior to the other in any way whatsoever – but without regard to the ‘facts’. However, Crampton & Parkin have found enough serious flaws in the methodologies of Lea & Chambers and similar researchers to cast doubt on the veracity of their findings. At present we are a long way off being clear whether there are real racial/ethnic differences in incidence of MAO-A-L and just how much it influences behaviour and under what environmental influences.
Interesingly tly Cases et al found that disabling the MAOA gene on the X chromosome of XY male mice made them highly aggressive – as per the ‘warrior gene’ effect. Cases et all were then able to restore the male mice to ‘normal’ behaviour by restoring the function of the MAOA gene on their X chromosome.
The difficulty in attempting to isolate the MAO-A-L allele as the cause of violence in such cases is illustrated by the work of Gregory Stuart et al (2014). In a study of 97 male batterers on a programme for treating intimate partner violence, they found this variation to be present in the most physically violent and verbally abusive. However, they also found an association between the violence and variations in the 5-HHT serotonin transporter gene.
There is some evidence that dopamine may also be involved with increases in aggressive behaviour. Jan Buitelaar (2003) found that the use of dopamine antagonists reduced aggressive behaviour in juvenile delinquents. However, as dopamine is critical to the coordination of movement, reduced aggressive behaviour as a result of lowered dopamine levels may be as much about movement being more restricted as reduced motivation to be violent. R Lavine (1997) associated increases in aggressive behaviour with increases in dopamine activity brought on by the use of amphetamines. Maria Couppis & Craig Kennedy (2008) found that, in mice, the meso-limbic pathway, the brain’s reward system, becomes engaged in response to an aggressive event, with dopamine involved as a positive reinforcer on this pathway. (Dopamine is well known as a key element on this pathway for such stimuli as food, sex and addictive drugs from nicotine to heroin.) These and similar findings led Couppis (2008) to state that dopamine plays an important reinforcing role in aggression. In other words, some people intentionally seek out aggressive encounters because of the rewarding sensations, caused by the increase in dopamine from these encounters.
Lending support to the role of dopamine, Wolfgang Retz et al (2003) found an association between a DRD3 variant (the gene for dopamine receptor D3) and both impulsivity and ADHD-related symptoms in violent offenders
While all the usual caveats need to be applied with regard to animal studies, a study by P F Ferrari et al (2003) lends support to the roles of both dopamine and serotonin in aggression. A rat was allowed to fight for 10 days at precisely the same time each day. On the 11th day the researchers did not allow the rat to fight at the usual time but examined it instead. They found elevated dopamine and reduced serotonin, indicating the rat’s brain chemistry had changed to facilitate the increased aggression required of it.
However, a meta-analysis by Angela Scerbo & Adrian Raine (1993) of 29 studies on anti-social children and adults published before 1992 found different results. The researchers found a consistent trend of lower levels of serotonin in aggressive individuals. However, they found no significant rise or fall in dopamine levels. Lower levels of serotonin were found in all the anti-social groups but they were particularly low in those who had attempted suicide.
Genes and neurophysiology
With regard to the question of which genes contribute to the development of criminal behaviour, from a 2014 meta-analysis Evangelos Vassos, David Collier & Seena Fazel could find no association between aggression and any one single gene. Michael Lyons (1995) postulates that potentially up to 100 genes may be involved. Michael Rutter (1995) makes the point that there is no such thing as a ‘criminal gene’. Rather particular genes may create the likelihood of certain behaviours.
There would be serious ethical concerns with deliberately breeding humans to see if more aggressive humans could be created; but Randy Joe Nelson (2006) has noted that selective breeding experiments can lead to more aggressive behaviour in animals. Kirsti Lagerspetz (1979) demonstrated this in mice which she selectively bred over 25 generations. In each generation she mated the least aggressive males and females with each other and the most aggressive males and females with each other. The result was one super-aggressive strain of mice and one very docile strain – thus demonstrating a notable genetic effect. That the genetic effect was greater than environmental influence was shown in an earlier study by Kirsti Lagerspetz & Kauko Wuorinen (1965) in which selectively-bred aggressive mice were cross-fostered to non-aggressive mothers and still demonstrated more aggressive behaviour than selectively-bred non-aggressive mice. However, R B Cairns, D J McCombie & K E Hood (1983) found that selectively-bred highly aggressive males and female mice showed this aggression more in middle age than when they were young or old. The implication of the mice being more aggressive when older is that, again, there may be an epigenetic effect at work.
Andreas Reif et al (2009) investigated the relationship between impulsivity and variants of the NOS1 gene, using a sample of psychiatric clinics which included 182 criminals. They found that the variant of NOS1 was more prevalent in adults with ADHD, some personality disorders and aggressive behaviour against both self and others. Reif et al found that the gene variant reduced activity in the anterior cingulate cortex (concerned with processing information about emotion and reward); they speculated that the variant of NOS1 may affect the control of impulsive behaviour often associated with aggression.
Research on smaller mammals has provided some interesting insights into the association of certain brain structures with aggressiveness. Philip Bard showed way back in 1929 that removal of the cortex in cats resulted in overt aggression but additional removal of the hypothalamus prevented it. In terms of modern neuroscience, these findings can be explained by removal of the cortex taking away the inhibition centres of the dorsal frontal cortex, thus meaning the affected cats would be unrestrained in their aggressive response to a provocation. In humans these dorsal front cortex inhibition centres have been associated by Mark Solms (2000) with Sigmund Freud’s Ego and Superego while the fMRI studies of Svenja Caspers et al (2011) would implicate these areas as being involved in the workings of the PURPLE and BLUE vMEMES – see A Biological Basis fior vMEMES? Further light on the role of the hypothalamus in aggression is shed by Allan Siegel & Claudia Pott (1988) who found that stimulation of the ventromedial hypothalamus in cats led to the spontaneous production of aggressive responses. Another key structure of the limbic system, the amygdala has been implicated in aggression. David Egger & John Flynn (1963) found that stimulating one part of the amygdala made cats aggressive while stimulating another part decreased aggressive behaviour. Several studies led by Michael Potegal have further implicated the amygdala. Michael Potegal et al (1996b) found that stimulating the corticomedial amgydala in hamsters produced aggressive behaviour. Michael Potegal et al (1996a) found that the corticomedial amygdala remained highly active in the 5-20 minutes ‘red alert’ period following stimulation. Potegal (1994) notes that humans have a similar 5-20 minutes ‘red alert’ period following provocation and, thus, supposes that the same area of the amygdala might be involved in human aggressive responses. Interestingly Solms associates the limbic systems with Freud’s impulsive and sometimes violent Id while Caspers et al’s fMRI scans seem to imply the limbic system is associated with the self-expressive vMEMES.
Using PET scans, Adrian Raine, Monte Buchsbaum & Lori LaCasse (1997) compared patterns of brain activity in people who had been convicted of murder or manslaughter with a sample of ‘normal’ controls, matched for age and sex. Of the 39 ‘murderers’, 2 were women and 6 had been diagnosed with Schizophrenia; this was also matched in the control group. Raine, Buchsbaum & LaCasse found reduced activity in both sides of the prefrontal cortex and in the amygdala, thalamus and hippocampus. In the thalamus and the areas surrounding the hippocampus, there was a difference in lateralisation: the murderers’ brains were much more active on the right than the left. The controls used both sides of the thalamus equally and the left side of the area surrounding the hippocampus more than the right. The researchers noted that the differences in the murderers’ brains could explain lack of fear, lowered self-control, increased aggression and impulsive behaviour and problems with controlling and expressing emotions. Such differences could lead to an increased risk of committing acts of extreme violence. They are also linked to problems with learning conditioned emotional responses and failure to learn from experiences. The effects on areas associated with learning could also mean lower IQ and, therefore, lower chances of employment and a higher risk of turning to criminal behaviour.
Earlier (1993) Raine used PET scans of the living brains of impulsive killers to find damage in the prefrontal cortex which is associated with controlling impulsive behaviour. (Raine’s technique involved watching a screen for 32 minutes and responding every time a zero appeared – with the impulsive individuals missing many of the zeros.) In 1982 Lorne Yeudall, Delee Fromm-Auch & Priscilla Davies had found that 90% of 2,000 persistent offenders in Canada had minor damage in the frontal or temporal regions of the brain.
Raine et al (1998) compared impulsive violent murderers with planned ‘predatory’ murderers, again using PET scans. They found that the impulsive murderers had lower prefrontal cortex functioning than the predatory murderers who had the same level of functioning as a control group. However, they had stronger sub-cortical functioning than the control group. The researchers concluded that the impulsive murderers lack the ability to regulate their emotional impulsivity.
Slow brain wave activity has been associated with Psychopathy. Robert Hare (1970) found that 14% of aggressive psychopaths showed slow wave activity in the temporal lobe, compared to 2% in the general population. However, Hare’s findings can only be considered correlational. Sarnoff Mednick et al (1981) took EEG readings of 600 Swedish children, both boys and girls, with no prior history of delinquency. 12 years later it was found that those with a slow brain wave pattern were more likely to have a police record. Although this was a prospective study, it still could only establish a correlation.
Lesser volume in the amygdala is also associated with Psychopathy. Yaling Yang et al (2009) compared 27 psychopathic persons with 32 controls, using MRI scans, They found the psychopaths had 17.1% less volume in the left amygdala and 18.9% less volume in the right amygdala. There was a significant negative correlation between lesser volume and more anti-social behaviour and less control. Andrea Glenn, Adrian Raine & Robert Schug (2009), using fMRI scans, found that psychopathic individuals had not just reduced amygdala volume but also reduced amgydala functioning during moral decision-making. Niels Birbaumer et al (2005) also found reduced amygdala activity in psychopaths undertaking a conditioning task, suggesting little fear or emotional response. This would make it easier to offend as these individuals are less capable of recognising or understanding the mental state of their victims.
Interestingly, Christian Keysers (2011) found that criminals with psychopathic tendencies only empathised (with a person in a film) when asked to. This finding suggests that in these people empathetic mirror neurons are not ‘switched on’ by default as they are in ‘normal’ people but have to be specifically activated by environmental stimulation.
Perhaps shedding some light on paedophilia, Boris Schiffer et al (2007) found male paedophiles had less grey-matter volume than comparison groups of heterosexual and homosexual men.