Neural, Hormonal and Genetic Explanations of Aggression

Biological explanations argue that aggression comes from inside the person: the structure and chemistry of the brain, the hormones circulating in the body, and the genes inherited from parents. Rather than looking to upbringing or situation, they locate the causes of aggressive behaviour in neural mechanisms, hormonal mechanisms, and genetic factors.

The AQA specification names three areas you must be able to describe and evaluate:

Explanation	Key factors on the spec
Neural mechanisms	The limbic system (including the amygdala), serotonin
Hormonal mechanisms	Testosterone
Genetic factors	Heritability from twin/adoption studies, the MAOA gene

These are not competing theories so much as layers of the same biological account. Genes shape the brain chemistry and hormone systems that then drive behaviour. A strong answer shows how they connect: for example, the MAOA enzyme regulates serotonin, so a genetic factor feeds directly into a neural mechanism.

The biological approach treats aggression as a product of neural, hormonal and genetic influences rather than learning or environment.

The limbic system is a set of subcortical structures involved in emotion, including the amygdala, the hypothalamus and the hippocampus. Within it, the amygdala is the structure most strongly linked to aggression because it is central to how we assess and respond to threat.

When the amygdala judges something in the environment as threatening, it triggers a rapid emotional and behavioural response. A more reactive amygdala is associated with greater aggression: the threat system fires more readily, so provocation is more likely to tip into an aggressive reaction.

Gospic et al. (2011) provided evidence for this. Using a provocation task (the Ultimatum Game) with fMRI, they found that when participants reacted aggressively to being treated unfairly, there was a spike in amygdala activity. A benzodiazepine drug that dampens arousal reduced both the aggression and the amygdala response, supporting a causal link.

The amygdala does not act alone. It is regulated by the prefrontal cortex, which normally applies the brakes. Weak prefrontal control over an over-reactive amygdala is the fuller picture of the neural basis of aggression.

Serotonin is a neurotransmitter that normally has a calming, inhibitory effect on the brain. It dampens neural activity in the prefrontal cortex, helping a person to control their impulses and think before acting.

The key exam point is the direction of the effect:

• Normal serotonin → the prefrontal cortex exerts good self-control → impulses are held in check.
• Low serotonin → this inhibition is reduced → the person is more likely to act on impulse → impulsive aggression becomes more likely.

So it is low serotonin, not high, that is linked to aggression. Low serotonin removes a natural brake on behaviour.

Drug (pharmacological) studies support this. Experimentally lowering serotonin levels increases aggressive responses, while drugs that raise serotonin activity tend to reduce them. For example, Berman et al. (2009) found that participants given the SSRI paroxetine (which increases serotonin) gave fewer and less intense electric shocks in response to provocation than a placebo group, but only among participants with a prior history of aggression.

Remember the mechanism: serotonin inhibits. Low serotonin means less inhibition, which means more impulsive aggression.

Testosterone is a male sex hormone (an androgen), produced in far larger amounts in males than females. It is linked to aggression and dominance behaviour, and its role is often used to help explain why aggression is more common in males and peaks in young adulthood, when testosterone is highest.

The strongest evidence comes from animal studies, which show a clear causal pattern:

Manipulation	Effect on aggression
Castration (removes testosterone)	Aggression falls
Testosterone injections restore levels	Aggression returns

In humans, the picture is weaker and mostly correlational — testosterone levels tend to be modestly associated with self-reported aggression or dominance, but you cannot ethically manipulate it, so causation is hard to establish.

The dual-hormone hypothesis refines this. It proposes that testosterone predicts aggression mainly when cortisol (the stress hormone) is low. High cortisol appears to inhibit testosterone's influence on aggressive behaviour. This shows the relationship is more complex than "more testosterone equals more aggression".

In the exam, be precise: testosterone's link to aggression is strong and causal in animals but modest and correlational in humans.

If aggression is partly biological, some of it should be inherited. Psychologists estimate the genetic contribution using twin studies (comparing identical MZ twins, who share ~100% of genes, with non-identical DZ twins, who share ~50%) and adoption studies (comparing adopted children with their biological versus adoptive relatives).

Findings from these designs suggest aggression is partly heritable. Coccaro et al. (1997) studied adult twin pairs and estimated that genetic factors accounted for around 50% of the variance in aggressive behaviour, with the environment explaining the rest.

Two points are essential for a good answer:

• Heritability of around 50% means genes matter and environment matters — neither alone explains aggression.
• Heritability describes variation across a population, not a fixed proportion within one individual.

No single "aggression gene" exists. Twin and adoption studies point to a general genetic vulnerability built from many genes interacting with the environment.

This general heritability sets up the specific gene AQA names: the MAOA gene.

The MAOA gene codes for the enzyme monoamine oxidase A (MAOA), which breaks down neurotransmitters — including serotonin — after they have been used. This is where genetics links directly back to the neural mechanism: if MAOA activity is abnormal, serotonin regulation is disrupted.

A low-activity variant, MAOA-L (nicknamed the "warrior gene"), is associated with higher aggression. Two key studies:

• Brunner et al. (1993) studied a large Dutch family in which many men showed impulsive, violent behaviour (including arson and assault). These men had a form of MAOA deficiency and abnormally low levels of the enzyme, linking the gene to aggression.
• Caspi et al. (2002) followed a large cohort and found that MAOA-L was linked to antisocial and aggressive behaviour only in men who had also experienced childhood maltreatment. Men with MAOA-L who were not maltreated did not show raised aggression.

Caspi's finding is a textbook example of a gene-environment (G×E) interaction: the gene raises risk only in combination with an environmental trigger.

Genotype	Maltreated in childhood?	Aggression risk
MAOA-L (low activity)	Yes	High
MAOA-L (low activity)	No	Not raised
High-activity variant	Yes	Not strongly raised

The MAOA gene is not deterministic. On its own it does not cause aggression; it changes how a person responds to their environment.

Serotonin has strong causal evidence, but is not the whole picture. Drug studies go beyond correlation: Berman et al. found that raising serotonin with paroxetine reduced aggression under provocation, supporting a causal role. However, aggression involves a network, not one chemical. The prefrontal cortex regulates the amygdala, and the amygdala interacts with hormonal and genetic factors, so reducing aggression to "low serotonin" is an oversimplification.

Testosterone evidence is mixed in humans. The animal evidence (castration and injection studies) is strong and causal, but human research is weaker, largely correlational, and often relies on self-reported aggression. The dual-hormone hypothesis shows the relationship depends on cortisol too, so the simple claim "more testosterone = more aggression" does not hold in people.

The MAOA gene is not deterministic. Most people carrying MAOA-L are not violent, and Caspi's work shows the gene matters only alongside an environmental trigger. This undermines any idea of a single "aggression gene" and shows aggression emerges from a gene-environment interaction rather than genetics alone.

Biological explanations risk being reductionist and deterministic. They can reduce a complex social behaviour to neurons, hormones and genes, ignoring cognitive and social factors (such as learning, provocation and disinhibition) that other explanations capture. There are also troubling real-world implications for legal responsibility: if aggression were purely genetic or neural, it raises difficult questions about whether offenders can be held responsible for their actions. (MAOA-L has in fact been raised in criminal-defence cases.) This is a strong reason to treat biological factors as one part of a fuller explanation.

1. Saying HIGH serotonin causes aggression

It is low serotonin that is linked to aggression. Serotonin is inhibitory and calming; low serotonin removes that inhibition, making impulsive aggression more likely. Writing "high serotonin" reverses the mechanism and loses the mark.

2. Calling MAOA-L an "aggression gene" that guarantees violence

MAOA-L raises risk only alongside an environmental trigger such as childhood maltreatment (Caspi et al.). Most carriers are not violent. Describe it as a gene-environment interaction, not a gene that determines aggression.

3. Treating the testosterone-aggression link as strong and causal in humans

The causal evidence is from animal castration and injection studies. In humans the link is modest and correlational, and the dual-hormone hypothesis shows it depends on cortisol. Do not overstate it.

4. Forgetting the amygdala is part of a wider network

The amygdala does not act in isolation. It is regulated by the prefrontal cortex and sits within the limbic system. Naming only the amygdala misses the network of limbic and prefrontal structures that AO3 credit rewards.

5. Describing genes and biology without any evaluation

Psychology essays are marked heavily on AO3. A description of the limbic system, serotonin, testosterone and MAOA without evaluation (reductionism, determinism, mixed human evidence, gene-environment interaction) caps the answer at a low band.