HookThe family that inherited a fault in an enzyme
In 1993 the geneticist Han Brunner published a study of a large Dutch family in which, across several generations, a striking number of the men shared a history of impulsive, violent behaviour — arson, assault, attempted rape — alongside mild learning difficulties. The women were unaffected. When Brunner sequenced their DNA he found a single mutation that knocked out the gene for monoamine oxidase A (MAOA), an enzyme that breaks down neurotransmitters including serotonin. Without it, the affected men could not regulate those chemicals normally. The press soon labelled the low-activity variant the 'warrior gene', which is exactly the trap this topic is designed to teach you to avoid — because a later study by Caspi found that the same gene raised the risk of antisocial behaviour only in men who had also been maltreated as children. The gene alone did almost nothing.
That tension — between a biological cause and everything that shapes whether it matters — runs through the whole of topic 4.15. You will meet the neural and hormonal machinery of aggression (the limbic system, serotonin, testosterone) and its genetic basis; the ethological account of aggression as an evolved instinct with its own triggers, and the evolutionary logic of human violence; three social psychological explanations (frustration-aggression, social learning theory, de-individuation); the special case of institutional aggression in prisons; and the modern question of whether media, and computer games in particular, make people more aggressive. The examiner rewards students who can move between the biological and the social without collapsing one into the other.
MechanismNeural, hormonal and genetic mechanisms
The limbic system — the amygdala above all — is the brain's threat detector, and its reactivity predicts aggression. Gospic used an Ultimatum Game inside an fMRI scanner: when participants were provoked by an unfair offer and retaliated, the amygdala fired; a benzodiazepine that dampens arousal reduced both amygdala activity and the number of aggressive rejections. Two chemicals modulate this circuitry. Low serotonin is linked to impulsive aggression because serotonin normally provides inhibitory control from the frontal cortex — take the brakes off and impulses run — with Virkkunen finding lower levels of a serotonin metabolite in the cerebrospinal fluid of violent impulsive offenders. Testosterone, a male hormone that acts on brain areas controlling aggression, is associated with dominance and violence; Dabbs found higher salivary testosterone in prison inmates convicted of violent rather than non-violent crimes.
The genetic strand is anchored by the MAOA gene from the hook. Because MAOA breaks down serotonin and other neurotransmitters, a low-activity variant (MAOA-L) leaves them poorly regulated. Twin and adoption studies show aggression is partly heritable, but the decisive finding is Caspi's gene-environment interaction: MAOA-L raised antisocial behaviour only in men who were also maltreated in childhood. That single result is the evaluative gold of this section — it shows that a purely biological, deterministic account is reductionist, because the gene's effect depends entirely on the environment. The other honest caution is direction of causation: winning a fight raises testosterone, so hormone levels may be a consequence of aggression as much as a cause.
ModelThe ethological and evolutionary explanations
The ethological explanation treats aggression as an adaptive instinct that helps animals space out over territory and establish dominance hierarchies without constant bloodshed. Its two technical terms are essential. An innate releasing mechanism (IRM) is a built-in neural circuit that, when triggered by a specific sign stimulus (or releaser), sets off a fixed action pattern (FAP) — a stereotyped, universal, innate sequence of aggressive behaviour that, once started, runs to completion (it is 'ballistic'). Tinbergen's sticklebacks are the classic demonstration: a male will attack any model with a red underside — the sign stimulus — however unrealistic, yet ignore an accurate model that lacks the red belly. Lorenz added that within a species aggression is often ritualised, ending in appeasement displays rather than death, which limits harm.
The evolutionary explanation applies the same adaptive logic to humans: aggression persists because, ancestrally, it paid off — securing resources and status, deterring rivals, and winning access to mates. Sexual jealousy is the flagship example. Because a man can never be certain of paternity, Wilson and Daly argued that male aggression and 'mate-retention' strategies (jealous mate-guarding, controlling behaviour) evolved to reduce the risk of cuckoldry, which is offered as one factor in patterns of intimate-partner violence. The evaluation to hold: the ethological account struggles to extrapolate from animal FAPs to flexible, learned human violence, and the evolutionary account is criticised as untestable 'just-so' storytelling and, on socially sensitive topics like partner violence, as potentially excusing behaviour — so it must be handled as a partial explanation, not a justification.
ModelSocial psychological explanations
Three social explanations sit together on the spec. The frustration-aggression hypothesis (Dollard) originally claimed frustration — being blocked from a goal — always leads to aggression, and aggression is always caused by frustration; the drive is relieved (cathartically) by aggressing, which may be displaced onto a safer, available target (a scapegoat) when the source cannot be attacked. Berkowitz reformulated it: frustration creates only a readiness for aggression (negative affect), and aggression actually occurs when environmental aggressive cues are present — his 'weapon effect' study found participants delivered more shocks when a gun was visible in the room than when a neutral object was.
Social learning theory (Bandura) argues aggression is learned by observation and imitation. In the Bobo doll studies children who watched an adult model attack the doll reproduced the aggression, especially with a same-sex model, and were more likely to imitate when the model was rewarded — vicarious reinforcement. Learning runs through the mediational processes (attention, retention, reproduction, motivation) and is shaped by self-efficacy — a child who finds aggression works becomes more confident using it. De-individuation explains aggression in crowds: immersion in a group brings anonymity and reduced private self-awareness, loosening the normal restraints on behaviour. Zimbardo found participants made anonymous by hoods delivered longer electric shocks than identifiable ones, and Rehm found handball teams dressed in identical strips played more aggressively. The neat evaluative link is that these three are not rivals — frustration can supply the trigger, SLT the learned method, and de-individuation the disinhibiting context.
CaseInstitutional aggression in prisons
Why are some prisons so much more violent than others? Two models compete, and the exam almost always wants them weighed against each other. The dispositional explanation — the importation model (Irwin and Cressey) — says aggression is carried into the prison: inmates import the values, traits and subcultural norms of the criminal world they came from, so a violent prison reflects the violent dispositions of the people locked inside it, not the walls around them. Gang membership, prior convictions and a history of violence predict institutional aggression, supporting importation.
The situational explanation — the deprivation model (Sykes) — says the institution itself generates aggression through the 'pains of imprisonment': the loss of liberty, autonomy, goods and services, heterosexual relationships and security. These deprivations create stress and frustration that erupt as violence, and factors like overcrowding, heat and poor management make it worse. Zimbardo's Stanford Prison study is the textbook situational evidence — ordinary students became abusive purely from the assigned role and environment. The evidence is genuinely mixed: importation predicts which individuals become violent, deprivation predicts which conditions produce violence, so the strongest answer treats them as complementary — an interactionist account in which imported dispositions are ignited by depriving situations.
MechanismMedia influences on aggression
The final leaf asks whether media — television, film and especially computer games — increase aggression, and it names three mechanisms you must be able to distinguish. Desensitisation is the reduction of the normal physiological and emotional response to violence through repeated exposure: watch or perform enough simulated violence and arousal drops, empathy dulls, and real aggression feels less shocking. Bartholow found habitual violent-game players showed a reduced brain response (a smaller P300 wave) to images of real violence, and this reduced arousal predicted more aggressive behaviour in a later task. Disinhibition is different: media that portrays aggression as normal, justified or rewarded weakens the social and moral restraints that usually hold it in check — the behaviour is not made less shocking so much as made to seem acceptable. Cognitive priming is different again: repeated exposure lays down aggressive 'scripts' in memory (Huesmann), and a later cue in the environment activates, or primes, that stored script, making an aggressive response more accessible and more likely.
The evaluation of media research is a topic in itself. Laboratory studies establish short-term causation but use artificial measures of 'aggression' (noise blasts, hot-sauce doses) with weak ecological validity; longitudinal studies capture real behaviour but cannot rule out that already-aggressive people simply choose violent media (the direction-of-causation problem); and the whole field is socially sensitive, feeding policy debates about game classification. The measured conclusion examiners reward is that media is one contributory risk factor interacting with dispositional and social ones — not a sole or sufficient cause of aggression.
A 16-mark essay asks you to 'discuss the influence of media on aggression'. A top-band evaluative paragraph: A strength of the media explanation is that its three mechanisms are supported by evidence at different levels. Bartholow's finding that habitual violent-game players show a reduced P300 response to real violence gives a physiological basis for desensitisation, and this reduced arousal statistically predicted greater aggression — a genuinely causal chain rather than a bare correlation. However, much of the supporting research is laboratory-based and operationalises aggression as noise blasts or hot-sauce allocation, which lack ecological validity and may not reflect real-world violence. Longitudinal studies address this but introduce a direction-of-causation problem: aggressive individuals may simply select violent media, so exposure could be a symptom rather than a cause. This suggests media is best understood not as a sole cause but as one contributory factor that primes and disinhibits aggression in people already made vulnerable by dispositional and social influences. Notice the marks: named evidence, a stated mechanism, a validity limitation, an alternative causal reading, and an interactionist conclusion that connects back to the rest of the topic.
VocabularyKey terms the mark scheme pays for
TrapsMisconceptions that cost marks
ExamWhat examiners want
Aggression is an optional Paper 3 topic, examined with short AO1/AO3 questions, application (AO2) scenarios and 16-mark essays graded over four levels (roughly 6 AO1 + 10 AO3). Because the topic spans biological, ethological, evolutionary and social explanations, the highest-scoring skill is cross-linking: use one explanation to evaluate another (e.g. SLT and the maltreatment effect on MAOA both show environment matters), and conclude with an interactionist synthesis rather than crowning a single 'winner'.
Name studies and their findings precisely — Gospic's amygdala/benzodiazepine result, Caspi's gene-environment interaction, Tinbergen's stickleback sign stimulus, Bandura's Bobo doll, Zimbardo's anonymity shocks, Bartholow's reduced P300. A named finding used as evidence earns AO3 credit that a generic assertion cannot. Reach for the issues-and-debates hooks the topic is built around: biological determinism and reductionism (the 'warrior gene'), nature-nurture (genes needing an environmental trigger), and social sensitivity (evolutionary accounts of partner violence, media-and-games policy) — always stressing that an explanation is not an excuse.
On application questions, anchor every point in the stem: if a scenario describes a calm person who becomes aggressive only in an anonymous crowd, name de-individuation and cite reduced private self-awareness and Zimbardo, then tie it explicitly to that character. The AO2 mark is for the link between theory and scenario, so quote the scenario back in your answer rather than describing the theory in the abstract.