Specification: Genetic factors in aggression, including the MAOA gene.

Aggression often seems to "run in families". This could be because family members share an environment, so children copy what they see at home. It could also be because family members share genes. Genetic explanations propose that some people inherit a greater tendency to behave aggressively than others.

There is no single "gene for aggression". Genes are instructions for making proteins, such as enzymes. These proteins affect how the brain works: for example, some enzymes break down neurotransmitters such as serotonin. A gene can therefore influence aggression indirectly, by changing the neural mechanisms that control it. Psychologists have investigated this in two ways: by comparing people who share different proportions of their genes (twin and adoption studies), and by looking for specific genes linked to aggression, especially the MAOA gene.

Key terms

• Concordance rate: the percentage of pairs (e.g. twins) in which, if one has a characteristic, the other has it too.

• Heritability: the proportion of the variation in a characteristic within a population that is due to genetic differences between people.

• MAOA gene: a gene on the X chromosome that codes for the enzyme monoamine oxidase A, which breaks down the neurotransmitters serotonin, dopamine and noradrenaline.

• MAOA-L: the low-activity variant of the MAOA gene, sometimes called the "warrior gene". People with it produce less of the enzyme. MAOA-H is the high-activity variant.

• Gene–environment (G×E) interaction: when the effect of a gene depends on the environment a person experiences.

• Diathesis-stress model: the idea that an inherited vulnerability (the diathesis) only leads to a behaviour when it is triggered by an environmental stressor.

• Polygenic: influenced by many genes, each with a small effect.

Twin studies

Twin studies compare two types of twins. Identical twins are monozygotic (MZ): they develop from one fertilised egg, so they share 100% of their genes. Non-identical twins are dizygotic (DZ): they develop from two eggs, so they share on average 50% of their genes. Both types of twins grow up in the same family at the same time, so researchers assume their environments are equally similar. If MZ twins are more similar in aggression than DZ twins, the extra similarity is assumed to be due to their extra shared genes. However, MZ twins look identical and are often treated more alike than DZ twins, so this "equal environments" assumption may not hold, and twin studies may overestimate the genetic contribution.

Key study: Coccaro et al. (1997)

Aim: To estimate how far different types of aggression are influenced by genes.

Procedure: The participants were 182 MZ and 118 DZ adult male twin pairs from the US Vietnam Era Twin Registry. Each twin completed a self-report questionnaire (the Buss–Durkee Hostility Inventory) measuring different types of aggression, including direct physical assault and verbal aggression. The researchers compared how similar the MZ twins were with how similar the DZ twins were.

Findings: MZ twins were more similar than DZ twins. Genetic factors accounted for 47% of the variation in direct physical aggression (about half) and 28% of the variation in verbal aggression. The rest of the variation was explained by the environment.

Conclusion: Physical aggression has a substantial genetic component. However, about half of the variation in physical aggression, and most of the variation in verbal aggression, is environmental.

Adoption studies

Adoption studies separate genes from environment. An adopted child shares genes with their biological parents but shares an environment with their adoptive parents. If adopted children are more similar in aggression to their biological parents, this suggests a genetic influence. If they are more similar to their adoptive parents, this suggests an environmental influence.

Rhee and Waldman (2002) carried out a meta-analysis combining the results of 51 twin and adoption studies. They concluded that genetic factors account for about 41% of the variation in aggressive and antisocial behaviour. Taken together with Coccaro et al. (1997), this suggests that genes explain a substantial part, but not all, of the differences in aggression between people.

The MAOA gene

The MAOA gene is the specific gene most strongly linked to aggression. It codes for an enzyme called monoamine oxidase A. After a neuron releases the neurotransmitters serotonin, dopamine and noradrenaline into the synapse, this enzyme "mops them up" by breaking them down, a process called metabolism. This stops the neurotransmitters from building up and keeps neural activity under control.

The gene comes in different versions. The low-activity variant (MAOA-L), sometimes called the "warrior gene", produces less of the enzyme. In people with MAOA-L, the neurotransmitters are not broken down efficiently, so their levels are abnormal. Each neurotransmitter is linked to a different part of aggressive behaviour:

• Noradrenaline: excess noradrenaline heightens the fight-or-flight response, so the person over-reacts to perceived threats.

• Dopamine: excess dopamine increases the rewarding feeling when aggressive acts are carried out.

• Serotonin: disrupted serotonin function is linked to a lack of inhibition over impulsive behaviour.

Because the MAOA gene is on the X chromosome, it affects males and females differently. Males (XY) have only one copy of the gene, so if it is the low-activity variant there is nothing to compensate for it. Females (XX) have two copies, so a normal copy on one X chromosome can make up for a low-activity copy on the other. This may help to explain why MAOA-linked aggression is seen mainly in males.

Key study: Brunner et al. (1993)

Aim: To investigate why many men in one large Dutch family showed violent, impulsive behaviour.

Procedure: This was a case study of one family. The researchers examined family records covering several generations and analysed urine samples and DNA from affected and unaffected men in the family.

Findings: Many of the men showed impulsive aggression, including arson, attempted rape and violent outbursts, as well as borderline intellectual disability. The affected men had a rare mutation in the MAOA gene, which meant they produced no working MAOA enzyme at all, and their urine showed abnormal levels of the neurotransmitters it normally breaks down. Women in the family were not affected.

Conclusion: A fault in the X-linked MAOA gene was associated with aggression, which is consistent with the gene's role in breaking down neurotransmitters. However, this was a single family with an extremely rare mutation, so the findings may not generalise to people with the much more common low-activity variant, and the family's shared environment may also have contributed to the men's behaviour.

Gene–environment (G×E) interactions

Having the MAOA-L variant does not mean that a person will inevitably become aggressive. Many people with MAOA-L are never violent. The effect of the gene depends on what happens to the person, especially in childhood. This is called a gene–environment interaction.

Frazzetto et al. (2007) identified which MAOA variant each of 235 adults carried, and asked them to complete questionnaires on their physical aggression and on traumatic events they had experienced in the first 15 years of life, such as family violence, the loss of a parent or sexual abuse. Men with the low-activity MAOA variant had higher physical aggression scores, but only if they had experienced significant early trauma. Men with the same gene variant who had not experienced early trauma were not especially aggressive. Women did not show this pattern.

These findings fit the diathesis-stress model. MAOA-L is the diathesis: an inherited vulnerability that makes aggression more likely. Early trauma is the stressor: an environmental trigger. Aggression is most likely when a person has both the vulnerability and the trigger, which explains why the gene alone does not predict who becomes aggressive.

Evaluation

The "warrior gene" label shows that genetic research on aggression is socially sensitive. Lea and Chambers (2007) used the term "warrior gene" when they suggested that the low-activity MAOA variant was more common among Māori men and linked this to a warrior past. Their claims were widely criticised as stigmatising, because they implied that a whole ethnic group was naturally prone to aggression. This shows how genetic findings about aggression can be used to stereotype groups of people who have done nothing wrong, and it ignores the environmental factors that research shows are needed to trigger the gene. Researchers therefore need to report genetic findings carefully, because labels such as "warrior gene" can cause harm well beyond the participants in a study.

Animal research provides experimental support for the role of MAOA. Godar et al. (2014) studied "knock-out" mice in which the MAOA gene had been deleted. These mice had raised serotonin levels and were hyper-aggressive. When the mice were given a dose of fluoxetine, a drug that acts on the serotonin system, their aggression was reduced. Because the gene was deliberately removed, this provides evidence of cause and effect that human correlational studies cannot provide, and it suggests that MAOA normally helps to keep serotonin, and therefore aggression, at normal levels. However, mouse aggression is far less influenced by learning and culture than human aggression, so the size of the genetic effect in humans may be much smaller. The findings support the MAOA explanation, but should be applied to humans with caution.

Aggression is likely to be influenced by many genes, not one. Stuart et al. (2014) studied 97 men in programmes for perpetrators of intimate partner violence. They combined two genetic risk factors, the low-activity MAOA variant and a variant of the serotonin transporter gene (5-HTTLPR), into a single genetic risk score. Men with a higher score showed more physical and psychological aggression towards their partners and inflicted more injuries, even after the researchers controlled for alcohol problems. This suggests that several genes affecting the serotonin system contribute to aggression together, each with a small effect. Explaining aggression through the MAOA gene alone is therefore reductionist. A polygenic explanation, in which many genes interact with each other and with the environment, is likely to be more valid.

It is difficult to isolate the effect of genes from the effect of the environment. Genes linked to aggression often only show their effect when the environmental conditions are right. McDermott et al. (2009) found that men with the low-activity MAOA variant behaved more aggressively than men with the high-activity variant in a lab task, by giving more hot chilli sauce to another player, but only when they had been provoked. This suggests that the gene did not cause aggression on its own: provocation was needed to trigger it. This makes it very hard to establish exactly how much influence genes have, because their effect depends on the situation. It supports a gene–environment interaction explanation rather than a purely genetic one.

Findings depend on how aggression is measured. Studies measure aggression in different ways, including self-reports, reports from parents and teachers, and observations. Rhee and Waldman's (2002) meta-analysis found that genetic factors had a greater influence in studies that used reports from other people, such as parents and teachers, than in studies that used self-reports. This suggests that heritability estimates partly depend on the measurement method rather than only on aggression itself. Because different methods produce different answers, it is difficult to compare studies or to pinpoint the true size of the genetic contribution. This reduces confidence in any single figure, even though the general conclusion that genes play some role is consistent across methods.

Research into prosocial behaviour supports the MAOA explanation, but also shows that social norms matter. If the low-activity variant increases aggression, the high-activity variant should be linked to less aggressive, more cooperative behaviour. Mertins et al. (2011) found exactly this: males with the high-activity MAOA variant were more cooperative, contributing more to the group in a lab-based money game, than those with the low-activity variant. This suggests that prosocial and antisocial behaviour may be two sides of the same genetic coin, which strengthens the MAOA explanation. However, Mertins et al. also found that the gene's effect became smaller as players were given more information about how much others were contributing. This suggests that social norms and other people's behaviour can override a genetic tendency, so genes are only part of the explanation.

Overall

There is consistent evidence that genetic factors contribute to aggression. Twin and adoption studies suggest that roughly 40 to 50% of the variation in aggression is inherited, and research on the MAOA gene identifies a specific mechanism through which genes can affect the neurotransmitters that regulate aggression. However, research such as Frazzetto et al. (2007), McDermott et al. (2009) and Mertins et al. (2011) shows that the effect of MAOA-L depends on early trauma, provocation and social norms. This means the genetic explanation implies only soft determinism: genes raise the risk of aggression but do not make it inevitable. This matters for the justice system, because a person with MAOA-L can still be held responsible for their actions and can change their behaviour. The most convincing conclusion is an interactionist one, in which genes create a predisposition that the environment then triggers or holds back.

Exam tips

• Keep the focus on genetics. In June 2022, examiners reported answers that "barely mentioned genetics but focused almost exclusively on neural explanations". Neural material is only relevant if you link it to its genetic basis (for example, MAOA → serotonin).

• For a 4-mark question on one genetic study, any genetic study is acceptable (Brunner, twin studies, knock-out mice), but studies of hormones are not credited.

• Know the mechanism precisely: the low-activity variant produces less enzyme and so leaves excess neurotransmitter, such as serotonin.

Possible Exam Questions 

1. Briefly outline and evaluate the findings of one research study into genetic factors in aggression. (4 marks) 

2. Outline and evaluate the role of genetic factors in aggression with reference to the MAOA gene. (16 marks)