Download UNIT TWO - BIOLOGICAL EXPLANATIONS OF AGGRESSION File

UNIT TWO: BIOLOGICAL THEORIES OF AGGRESSION
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1. Genetic factors
2. Neural mechanisms and aggression
3. Hormones and aggression
1. Genetic factors
Learning objective: You will be able to:

Outline and evaluate: genetic – neural – hormonal factors in aggression
Genes do not directly cause aggression. Genes influence elements of our biology that contribute to it.
Selective breeding involves choosing animals with desirable characteristics and mating them with similar other animals in
order to enhance these particular traits. Selective breeding of some animals for aggression has been carried out for many
years. For example, Spanish fighting bulls, chickens (fighting cocks), fish (Siamese fighting fish), and dogs (pit bull terriers)
have all been selectively bred for high levels of aggression. The structural influence of genes on aggression can be seen in
all these animals, for example, the fighting cock is larger, has much stronger wing muscles and legs, and well developed
claws for damaging opponents.
There have been many laboratory –based selective breeding studies. One of the most influential has been by Lagerspetz
(1979), carried out in Turku, Finland. She isolated mice immediately after weaning. Mice reared in isolation tend to be
aggressive when later placed with other mice. Based on ratings of aggression when placed with another mouse (such as
attacking, biting response, speed) she classified them as either Turku aggressive (TA) or Turku non-aggressive (TNA). These
mice were interbred so that by the nineteenth generation rates of aggressive biting behaviour in the TA mice were 52%
compared to just 5% in TNA mice. It was also noted that the TA mice had heavier testes and forebrains and altered levels of
the neurochemical serotonin in the forebrain and noradrenaline in their brainstem, supporting the notion that genes
influence both the structural and functional aspects of an animal’s biology.
Lagerspetz (1981) does make the point however, that genetic factors do not absolutely determine aggressive behaviour,
but that environmental factors are also very important. For example, she points out that both strains of mice can be
conditioned to make them less aggressive.
However, understanding the influence of genes on human aggression is a much more difficult task than it is with lower
animals. Not only are humans much more complex organisms because of our highly evolved brains, but we live in complex
environments which influence behaviour in many and often unpredictable ways. Discriminating between genetic and
environmental influences is very difficult. Whilst selective breeding and rearing in isolation might theoretically address the
problem it is obviously not practical or ethical to do so with humans. An alternative approach has been to investigate a
naturally occurring population with known genetic factors – identical (or monozygotic, MZ) twins. Because they are
genetically identical, any similarities in aggressiveness might be attributable to shared genes, whilst differences in
aggression between them could be ascribed to environmental variables. A strong argument could be made for genetic
components in aggression, if MZ twins separated at an early age and reared apart (hence having different environments)
were found to have similarities in aggression.
Findings from twin studies however have been extremely variable. For example, Canter (1973) found a correlation of 0.14
for MZs reared together, whilst for the same kind of population O’Connor (1980) found a correlation of 0.72. Slightly less
variability emerges from the analysis of correlations in aggressiveness of MZ twins reared apart. However, whilst the
correlations vary, what remains constant across all studies is a greater association of aggressiveness with MZ than with DZ
(non-identical twins) whether reared together or apart (see table below) this is strongly indicating a genetic contribution,
even if there is disagreement about its magnitude.
Identical twins (MZ)
Reared together
Reared apart
0.72
0.64
0.39
0.46
0.14
0.53
Non-identical twins (DZ
Reared together
Reared apart
0.42
0.34
0.42
0.06
0.30
0.39
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From a meta-analysis of twin and adoption studies, Miles and Carey, (1997) suggest a heritability measure of aggression of
50%. This is a very high estimate compared to an earlier meta-analysis of eleven twin studies by Plomin et al (1990), who
found a small heritability for aggression. The average concordance rate for MZ twins was 0.32and for DZ twins was 0.14. it
appears that different sources of evidence produce different estimates of the heritability of aggression. Rhee and
Waldman (2002) suggest that the variability may be due at least in part to the methods of assessing aggressive behaviour
in the various studies. Their meta-analysis of 51 twin and adoption studies indicated significant differences in the
magnitude of genetic and environmental effects according to how aggression was measured. They found that heritability
varied according to the assessment method used, with 39% for self-reported aggression and 53% when reported by others.
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Table summarising correlations for MZ and DZ twins reared together and apart. Adapted from Miles and Carey (1997)
UNIT TWO: BIOLOGICAL THEORIES OF AGGRESSION
.
1. Genetic factors
2. Neural mechanisms and aggression
3. Hormones and aggression
Genetic factors
The XYY syndrome
Some of the earliest efforts to determine the genetic basis of aggression involved studying the
XYY syndrome. This is where men have an extra Y male sex chromosome. Since males are
considered more aggressive than females, having an extra male chromosome suggests that XYY
males might be more aggressive. Jacobs et al (1965) found that the incidence of XYY syndrome
among inmates of institutions was approximately 3% whereas it is only 0.1% in the normal
population. This suggests that XYY males are more likely to engage in criminal acts than non XYY
males. Further studies indicated that these men were taller, and had lower levels of intelligence
than non-XYY males.
Whilst the link between XYY and aggression was widely accepted, a number of researchers
challenged the relationship. A wide scale study by Witken et al (1976) could find no link between
XYY syndrome and increased aggressiveness. They did however support previous findings that XYYs had lower levels of
intelligence. Whilst they were more likely to commit crimes, closer inspection of their offences showed that their crimes
were generally not violent in nature. The criminal records also revealed that XYYs were often not very good at being
criminals. Witken concluded that their lower IQ made them more likely to get caught and convicted for their crimes which
resulted in the higher proportion of XYY males in the prison population. Whilst Witken et al seem to successfully disclaim a
causal link between XYY syndrome and aggression, a role for XYY syndrome in aggression cannot be entirely discounted.
MAOA gene and aggression
Attention has turned recently to the issue of identifying particular genes underlying aggressive behaviour. Most recent
research has focused on a gene called monoamine oxidase A (MAOA) , since a number of studies have found a link
between this gene and aggression. MAOA gene regulates an enzyme in the brain also called monoamine oxidase A
(enzymes are substances in the body that either break down molecules or join others together). This enzyme is known to
break down several neurotransmitters, such as serotonin, noradrenaline, and dopamine. By removing excess amounts of
these neurotransmitters, monoamine oxidase A helps neurons to communicate with each other more efficiently. The
association with aggression makes sense because research has already established that these neurotransmitters are
related to mood, and a build-up of these chemicals can cause people to respond excessively (and often aggressively) to
stressful situations.
Studies with humans have indicated a link between MAOA gene and aggression. Brunner et al (1993) discovered a
mutation in the MAOA gene in a Dutch family. Family records showed a history of violence in only male members, often
associated with stressful events. Investigation indicated that the defective MAOA gene was passed onto problem men from
the X (female) chromosome of their mothers. The aggressive problem only affects men since they have only one X
chromosome, so show symptoms whenever they inherit the gene. Even though women too might inherit the gene, they
don’t show aggressive symptoms as they have a second X chromosome carrying a good copy of the gene. This is supported
in ground-breaking research by Cases et al (1995). They disabled the MAOA gene in an X chromosome of mice and found
that males became highly aggressive. Females were unaffected by the procedure. Whereas males lacked the monoamine
oxidase A enzyme, thereby increasing levels of dopamine and serotonin, females still had a functioning gene in their other
X chromosome to do the job.
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In a large longitudinal study of 1,037 children followed over 25 years, Caspi et al (2002) found that males who had been
severely maltreated as boys were more likely to engage in anti-social behaviour, including violence as adults. However,
males with the MAO-L gene were more than twice as likely to have been diagnosed in adolescence with a conduct disorder
as were those with the MAOA-H gene, and three times more likely to have been convicted of violent crime by 26 years of
age. While only 12% of the sample had a combination of maltreatment and the MAOA-L gene, this group was found to
have committed 44% of the crimes. The results indicate the importance of an interaction between genes and
environmental influence (nature-nurture). Having only one of the factors (MAOA-L gene or experience of maltreatment)
alone predicted later aggressive behaviour, but having them both did.
Research has suggested that the MAOA-L variant may be linked to structural changes in the brain. Meyer-Lindber et al
(2006) conducted an fMRI study using healthy participants. They found significant reductions in volume of several areas of
the brain including the amygdala and prefrontal cortex in MAOA-L compared to MAOA-H participants. These structures are
known to be involved in emotion and are often found to be impaired in anti-social individuals. Furthermore, McDermott et
al (2008) showed that participants in their study with the MAOA-L gene displayed higher levels of aggression in response to
provocation than those with MAOA-H variant. This appears to be evidence for a direct link between genetic varioation and
willingness to engage in acts of physical aggression.
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Different forms of the MAOA gene have been identified. One form of this gene is a low-activity one (MAOA-L) which
produces less of the monoamine oxidase. There is also a high-activity form of this gene (MAOA-H) which produces more of
this enzyme. Research suggests that it is having the MAOA-L gene in particular which predisposes an individual to antisocial and aggressive behaviour.
UNIT TWO: BIOLOGICAL THEORIES OF AGGRESSION
.
1. Genetic factors
2. Neural mechanisms and aggression
3. Hormones and aggression
2. Neural Mechanisms and Aggression
Research in the 1930s pointed to the involvement in emotional behaviours, including aggression, of a circuit of
structures deep in the brain (Pepez, 1937). Whilst some of the structures identified by Papez and others are no
longer considered as important in aggressive behaviour, subsequent research has clearly indicated key role for
several of them. Decades of research with non-human animals is beginning to lead to a consensus of opinion
that normal aggressive behaviour is not dependent on separate and independently functioning brain areas but
on the interaction of a system of structures. Specifically, there is a circuit of brain structures involved in
aggression running from the areas of the amygdala, down to the hypothalamus, and from there to the
periaqueductal grey (PAG) (Balir and Charney, 2003). This system appears to be organised in a hierarchical
way, so that aggressive responses originating higher up the circuit depend on those structures below
functioning normally, while those structures lower down the circuit do not depend on the functioning of those
higher up. For example, aggressive responses produced from the amygdala depend on the normal functioning
of the hypothalamus and PAG, but the PAG does not depend on the normal operation of the hypothalamus
and amygdale. At the highest level of control, this circuit appears to be moderated by the prefrontal cortex. It
is the role of the prefrontal cortex to control the outward expression of aggression. Research suggests that this
circuit works in a similar way to control human aggression. For example, structures within this circuit appear to
be involved in psychiatric disorders where there is a heightened risk of aggression, and damage due to such
things as stroke or tumour growth also produces changes in aggressive behaviour. Most research has focused
on the role in aggression of two of these structures in particular – the amygdala and the prefrontal cortex.
The role of the amygdale in aggression
Other research studies for you to look at if you
are interested are:
Narabayashi et al (1972)
Mark and Ervin (1970)
Ashford (1980)
Birbaumer et al (2005)
Amygdala
Periaqueductual grey (PAG)
The role of the prefrontal cortex in human aggression
The prefrontal brain regions are directly connected with limbic system structures
(the location of the hypothalamus and amygdala). They are thought to regulate the
amygdala-driven emotional responses and in this way exercise some form of
emotional control. Damage to the prefrontal cortex results in a range of responses,
including loss of control, impulsivity, immaturity, and altered emotionality all of
which are associated with aggressive acts (Damasio et al, 1994). Anderson et al
(1999) have shown that individuals with damage to the frontal cortex during infancy
are at an increased risk of aggressive behaviour as adults. Neuroimaging studies
have consistently found reductions in prefrontal brain tissue in people with antisocial and aggressive tendencies. Particular subgroups of aggressive individuals have
been found to have impaired functioning of the prefrontal cortex. Raine et al (1997)
for example investigated the brain activity of 41 murderers using positron emission
tomography (PET) scans. They found reduced activity in the prefrontal cortex. This is
also a critical area for learning, memory and attention. This fits in with suggestions
that violent offenders have difficulty in forming conditional emotional responses
and learning from experience (e.g. Cleckley, 1976). This research is also supported
by Soderstrom et al (2000) who found frontal and temporal lobe dysfunction in
impulsive and violent prisoners. Volkow et al (1995) looked at the cerebral blood
flow (CBF) of eight violent psychiatric patients. They found that, compared to
normal controls, the psychiatric patients had reduced cerebral blood flow
14to the
prefrontal cortex. It is possible this contributed to the repetitive, violent behaviour
of the patients.
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In a study of aggressive patients with temporal
lobe epilepsy, Van Elst et al (2000) found that
the amygdala had lost 20% of its volume.
Prefrontal cortex
Hypothalamus
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The amygdala has long been associated with
aggressive behaviour in both animals and
humans. One of the earliest links was
established by Kluver and Bucy in the 1930s
when they removed part of the temporal lobes
of rhesus monkeys thus destroying the
amygdala. The behavioural changes resulting
from this procedure (known as the Kluver-Bucy
syndrome) included a loss of fear and a marked
taming effect. Sustained electrical stimulation
of the amygdala in laboratory animals usually
results in fear and rage responses (LeDoux,
1996).
Humans have been found to behave similarly in
response to stimulation. A number of studies
have found that the size of the amygdala is
reduced in criminals with violent tendencies
(e.g. Wong et al, 1997).
UNIT TWO: BIOLOGICAL THEORIES OF AGGRESSION
.
1. Genetic factors
2. Neural mechanisms and aggression
3. Hormones and aggression
3. Hormones and Aggression
Observations of behaviour across many species reveal that aggression more often occurs in males than females. This sex
difference in aggression is usually attributed to the effects of the male sex hormone, testosterone. It is one of a class of
hormones called androgens which are important in producing sperm and developing secondary sexual characteristics.
These hormones also exert an influence on a range of behaviours, including aggression.
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Castration has been used as a technique for making domestic and farm animals more
manageable for many years, although the causal link between the effects of this surgery
and testosterone were not known until relatively recently. Early observations of animals
noted the relationship between testosterone and increased aggression in various species, especially at mating season, and
laboratory studies later established the involvement of testosterone in increased aggression at puberty. Beeman (1947)
castrated male mice and found that their aggressiveness reduced. He demonstrated the important role of testosterone in
producing this behaviour by later injecting the mice with testosterone and re-establishing their aggressiveness. Subsequent
studies however found that castration in mice only reduces aggression if it is done before puberty which is the age at which
the animal begins to behave aggressively. It seems that testosterone contributes to the development of aggression and
once it has accomplished this, its effects become relatively permanent and relatively unaffected by the subsequent loss of
testosterone.
The role of testosterone is clear in the behaviour of lower animals, but there is strong evidence that it contributes to
human aggression too. For ethical reasons androgens cannot be given to humans to see if changes in aggression occur. An
alternative approach has been to investigate testosterone levels in people who are displaying aggressive behaviours. Dabs
et al (1995) investigated the relationship between test, crime and prison behaviour. They measured the test in the saliva of
692 of male prisoners and found that those who had committed crimes of sex and violence had higher test levels. The high
test males also violated more prison rules involving confrontation. In another study Dabs 1996 looked at the relationship
between test and fraternity behaviour. Their argument was that since people affiliate with like minded others, then high
test levels may be a characteristic of groups as well as individuals. Shared interests and activities may serve to intensify
pre-existing characteristics. They measured the test levels of 240 members of 12 fraternities in 2 universities and compared
this to descriptions of fraternity behaviour. They found less smiling and generosity and lower academic achievement in the
high test fraternities. Members of fraternities with highest levels of testosterone were described as boisterous and macho
while those in the low testosterone fraternities were attentive and helpful.
There are many problems with studies such as these which investigate testosterone levels in individuals who may be
displaying aggressive behaviour. Firstly, this kind of research is correlational and correlations do not establish cause and
effect. They just show a relationship. Secondly, measurements of aggression are often unreliable, as behaviours are open
to interpretation. In Dabs’ fraternity study, for example, a lack of smiling was deemed a negative trait associated with being
less friendly. Clearly, smiling occurs for many reasons as does a lack of it which may not necessarily be attributed to
aggression. Furthermore, aggression can occur for many reasons other than hormone levels. Whilst women have less
testosterone than men its effects are considered to be the same. Dabs et al 1988 looked at the criminal history and looked
at the levels of 84 female prison inmates and found a relationship with criminal violence although this relationship was not
straightforward. Testosterone was highest in cases of unprovoked violence but lowest where violence was defensive (for
example abused wives who had retaliated). Dabs et al point out that this seems at odds with the findings of Olweus 1983
who reported higher testosterone levels in participants engaged in what could be called defensive aggression. This raises
the problem issue in aggression research of how exactly aggression is operationalised. Olweus, for example referred to
‘provoked’ aggression when participants were frustrated or restricted in some way. In fact, most of the inmates in the Dabs
et al study could be considered to have been provoked to violence, by either other people or circumstances.
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Noting the differences in aggressiveness in female laboratory rates, Vom Saal (1983) investigated the possibility that this
was due to their in-utero experience (experience in the womb). Rats can have around twelve young at a time, which are
positioned close together in two rows in the womb. Those gestating closest to the ovaries would be exposed to more
oestrogen (female hormone) than those lying further away. Also, those female rats
gestating next to brothers would be exposed to testosterone as the testes of their
brothers developed. He found that when they were born the female rats which gestated
closest of male rats were the most aggressive of the female rats in the litter.