Discuss the genetic factors in aggression (8 marker)
Several twin studies have suggested that genetic factors play a significant role in aggression, for
about 50% of the variance in aggressive behaviour. For example, Coccaro et al (1997) studied
aggressive behaviour, defined as direct physical assault, in male adult twin pairs. Coccaro found that
MZ twins had concordance rates of 50%, compared to DZ of 19%. This suggests a genetic component
to aggression as MZ twins share 100% of their genes, compared to DZ twins who only share 50% of
their genes. In addition, adoption studies can help to untangle the nature and nurture debate. The
corresponding figures for verbal aggression were 28% in monozygotic twins and 7% in dizygotic
twins.
If there is a purely genetic cause to aggression, adopted children should act as aggressive as their
biological parents. Hutchings and Mednick (1975) studied over 14,000 adoptees in Denmark and
found that a significant number of boys with criminal convictions also had biological fathers with
criminal convictions. Additionally, Rhee and Waldman (2002) carried out a meta-analysis of adoption
studies of direct aggression and antisocial behaviour, a prominent feature of which is aggressive
behaviour. They found that genetic influences accounted for 41% of the variance in aggression,
which is more or less in line with the findings of twin studies.
Furthermore, the MAOA gene controls the production of an enzymes called monoamine oxidase A.
MAO-A regulates the neurotransmitter serotonin, which is a monoamine thought to play an
important role in aggression. Genes come in different variants. The MAOA-L results in low activity of
the MAO-A enzyme and this has been linked to high levels of aggressive behaviour. The MAOA gene
has been nicknamed the “warrior gene’ because of research by Lea and Chambers (2007) who found
that the MAOA-L variant was possessed by 56% of New Zealand Maori men. Furthermore, the link
between the MAOA-L and aggression was further cemented by Brunner et al (1993).
(A further genetic explanation is that a mutation in the gene responsible for producing the protein
MAOA can lead to aggressive behaviour. MAOA regulates the metabolism of serotonin in the brain,
which is associated with social decision-making. Low levels of MAOA lead to low levels of serotonin,
which can lead to an increased susceptibility to act aggressively and impulsively).
This evidence demonstrates that genes are crucial influences on aggressive behaviour, but they do
not function in isolation. It appears to be that MAOA-L gene activity is only related to adult
aggression when combined with traumatic life experiences. Frazzetto et al (2007) found an
association between higher levels of antisocial aggression and the MAOA-L gene variant in men, but
this was only the case in those who had experienced significant trauma during the first 15 years of
life, which suggests strong evidence of gene-environment interaction.
One strength is research support for the role of the MAOA gene in aggression. Brunner (1993)
studied a Dutch family in which 28 males behaved very aggressively and violently. The men were
found to have MAOA-A and a defect in the gene responsible for making this protein was later
identified. Stuart et al (2014) found that 97 men convicted of intimate partner violence had the
MAOA-L variant gene and were the most violent perpetrators which resulted in the worst injuries on
their partners. This is a strength as these studies support the role of genetic factors in aggression,
more specifically the relationship between the MAOA gene activity and higher levels aggression,
increasing the validity of the genetic explanation for aggression.
However, one limitation of this contradictory research. Mertins et al also showed that non genetic
factors are crucial. They found that even participants with the MAOA-L variant behaved co-
operatively rather than aggressively when they were made aware that others in the study were
Several twin studies have suggested that genetic factors play a significant role in aggression, for
about 50% of the variance in aggressive behaviour. For example, Coccaro et al (1997) studied
aggressive behaviour, defined as direct physical assault, in male adult twin pairs. Coccaro found that
MZ twins had concordance rates of 50%, compared to DZ of 19%. This suggests a genetic component
to aggression as MZ twins share 100% of their genes, compared to DZ twins who only share 50% of
their genes. In addition, adoption studies can help to untangle the nature and nurture debate. The
corresponding figures for verbal aggression were 28% in monozygotic twins and 7% in dizygotic
twins.
If there is a purely genetic cause to aggression, adopted children should act as aggressive as their
biological parents. Hutchings and Mednick (1975) studied over 14,000 adoptees in Denmark and
found that a significant number of boys with criminal convictions also had biological fathers with
criminal convictions. Additionally, Rhee and Waldman (2002) carried out a meta-analysis of adoption
studies of direct aggression and antisocial behaviour, a prominent feature of which is aggressive
behaviour. They found that genetic influences accounted for 41% of the variance in aggression,
which is more or less in line with the findings of twin studies.
Furthermore, the MAOA gene controls the production of an enzymes called monoamine oxidase A.
MAO-A regulates the neurotransmitter serotonin, which is a monoamine thought to play an
important role in aggression. Genes come in different variants. The MAOA-L results in low activity of
the MAO-A enzyme and this has been linked to high levels of aggressive behaviour. The MAOA gene
has been nicknamed the “warrior gene’ because of research by Lea and Chambers (2007) who found
that the MAOA-L variant was possessed by 56% of New Zealand Maori men. Furthermore, the link
between the MAOA-L and aggression was further cemented by Brunner et al (1993).
(A further genetic explanation is that a mutation in the gene responsible for producing the protein
MAOA can lead to aggressive behaviour. MAOA regulates the metabolism of serotonin in the brain,
which is associated with social decision-making. Low levels of MAOA lead to low levels of serotonin,
which can lead to an increased susceptibility to act aggressively and impulsively).
This evidence demonstrates that genes are crucial influences on aggressive behaviour, but they do
not function in isolation. It appears to be that MAOA-L gene activity is only related to adult
aggression when combined with traumatic life experiences. Frazzetto et al (2007) found an
association between higher levels of antisocial aggression and the MAOA-L gene variant in men, but
this was only the case in those who had experienced significant trauma during the first 15 years of
life, which suggests strong evidence of gene-environment interaction.
One strength is research support for the role of the MAOA gene in aggression. Brunner (1993)
studied a Dutch family in which 28 males behaved very aggressively and violently. The men were
found to have MAOA-A and a defect in the gene responsible for making this protein was later
identified. Stuart et al (2014) found that 97 men convicted of intimate partner violence had the
MAOA-L variant gene and were the most violent perpetrators which resulted in the worst injuries on
their partners. This is a strength as these studies support the role of genetic factors in aggression,
more specifically the relationship between the MAOA gene activity and higher levels aggression,
increasing the validity of the genetic explanation for aggression.
However, one limitation of this contradictory research. Mertins et al also showed that non genetic
factors are crucial. They found that even participants with the MAOA-L variant behaved co-
operatively rather than aggressively when they were made aware that others in the study were
