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The oldest question in criminology is also its most dangerous: are some people made to offend by their biology? For most of the twentieth century, respectable social science answered "no" — crime was about poverty, upbringing and opportunity, and to look for it in the brain was to flirt with the discredited biological determinism of the nineteenth century. Then, in 1997, Adrian Raine and colleagues published brain scans of murderers that reopened the question with modern neuroscience. This lesson is the first topic of the OCR criminal option and the first to follow the applied three-strand format. In Background we survey physiological and non-physiological explanations of why some people become criminal. In Key research we study Raine, Buchsbaum and LaCasse's (1997) PET study of murderers pleading not guilty by reason of insanity, in the depth the exam requires — aim, sample, procedure, findings and the crucial limits on what it shows. In Application we design a biological strategy for preventing criminal behaviour. Throughout, the debates of nature–nurture, reductionism and determinism are never far away, because this is the topic where they bite hardest.
| This lesson covers | OCR H567 Component 03, Section B (Criminal) topic | AO focus |
|---|---|---|
| Physiological explanations of criminal behaviour (brain, genes, neurochemistry) | What makes a criminal? — Background (Biological) | AO1; AO3 evaluation |
| Non-physiological explanations (upbringing, learning, cognition) | What makes a criminal? — Background | AO1; AO2 comparison |
| Key research: Raine et al. (1997) PET brain abnormalities in murderers | What makes a criminal? — Key research | AO1 method/results; AO3 evaluation |
| A biological strategy for preventing criminal behaviour | What makes a criminal? — Application | AO2 application; AO3 judgement |
The specification is referenced descriptively throughout; consult the official OCR H567 specification document for the exact published wording. This lesson develops AO1 (knowledge of biological and non-biological explanations and of Raine et al.'s study), AO2 (applying the biological account to a prevention strategy) and AO3 (evaluating the study's method and the wider explanation for reductionism and determinism).
Physiological (biological) explanations locate the roots of criminal behaviour in the body — in the brain, the genes, the nervous system and biochemistry. Several strands are relevant.
The most direct claim is that abnormalities in specific brain regions predispose people to antisocial or violent behaviour. The prefrontal cortex, the region behind the forehead, is central to executive functions — planning, self-control, impulse regulation, and the inhibition of aggression driven by deeper, more primitive structures. If the prefrontal cortex is underactive or damaged, the brakes on aggression may fail. The limbic system — especially the amygdala (which processes fear, threat and aggression) and the hippocampus (memory and the regulation of emotional responses) — is implicated in the generation and control of aggressive impulses. The classic historical illustration is Phineas Gage, the nineteenth-century railway worker whose personality reportedly changed from responsible to impulsive and antisocial after an iron rod destroyed much of his prefrontal cortex — a case long used to argue that this region governs social self-control.
Behaviour-genetic studies ask whether a predisposition to offend is heritable. Twin studies comparing identical (monozygotic) and non-identical (dizygotic) twins, and adoption studies comparing adoptees with their biological and adoptive parents, have suggested a genetic contribution to antisocial and criminal behaviour — though the effect is partial, and shared environment matters too. Attention has focused on genes affecting neurotransmitter systems; the gene encoding monoamine oxidase A (MAOA), an enzyme that breaks down neurotransmitters, has been dubbed (misleadingly) the "warrior gene", with a low-activity variant linked to aggression — but, importantly, mainly in interaction with childhood maltreatment. That interaction is itself the strongest evidence against simple genetic determinism.
Low levels of the neurotransmitter serotonin (which normally dampens impulsive aggression) and abnormal levels of dopamine and the hormone testosterone have been associated with aggression and antisocial behaviour. There is also evidence around autonomic under-arousal: some persistently antisocial individuals show lower resting heart rate and reduced physiological reactivity, which may mean they are less responsive to punishment and seek stimulation through risk — a strand associated with the broader idea of a fearless, under-aroused temperament.
A balanced account must set the biology against explanations that locate crime outside the individual body — the "nurture" side of the debate, and a rich source of AO3 evaluation.
Learning and upbringing. Social learning theory (recall Bandura from Component 02) holds that aggression and offending can be learned by observing and imitating models — parents, peers, media — especially where the behaviour is seen to be rewarded. Operant conditioning adds that offending which is reinforced (by money, status or peer approval) is repeated. Harsh, inconsistent or neglectful parenting, and exposure to violence, are among the most robust predictors of later offending.
Social and economic factors. Poverty, inequality, poor housing, unemployment and living in high-crime neighbourhoods are all associated with elevated offending — the situational and sociological account that the "broken windows" topic develops.
Cognitive factors. Offenders, on average, show distinctive patterns of thinking: hostile attribution biases (reading neutral acts as hostile), poor moral reasoning, and cognitive distortions that minimise or justify harm.
The crucial evaluative point is that these are not rivals to be chosen between but interacting influences. The MAOA findings are the exemplar: the "risk" gene raises the probability of antisocial outcomes chiefly in those who were maltreated as children. Biology loads the gun; environment, for many theorists, pulls the trigger — and even that metaphor is too deterministic for the fully interactionist position most researchers now hold.
It is worth dwelling on why the interactionist position has become the mainstream, because doing so sharpens the evaluation. Purely genetic accounts founder on the fact that heritability is never total: identical twins, who share all their genes, are far from perfectly concordant for criminality, so genes cannot be the whole story. Purely environmental accounts founder on the opposite fact: children raised in the same adverse conditions diverge widely, some offending and most not, so environment cannot be the whole story either. The gene–environment interaction resolves this by proposing that the same environment has different effects depending on the person's biology, and the same biology has different effects depending on the environment. There is also gene–environment correlation: a temperamentally difficult, impulsive child may evoke harsher parenting (an evocative correlation) and may select more deviant peer groups as they grow older (an active correlation), so nature and nurture are not even cleanly separable — biology helps shape the very environment that then shapes behaviour. For the exam, the payoff is a ready-made critique of any one-sided explanation: whenever a source leans hard on biology or hard on upbringing, the sophisticated response is to show how the two are entangled.
A further strand of physiological explanation deserves note because it bridges to the study ahead: evolutionary accounts. From an evolutionary perspective, some aggression and acquisitiveness may be understood as strategies that, in ancestral environments, could increase status, resources or reproductive success. Such accounts are speculative and hard to test, and they risk the naturalistic fallacy (treating "natural" as "acceptable"), but they are part of the biological toolkit and a legitimate object of evaluation. The point for now is that "physiological explanation" is not a single claim but a family — brain, genes, neurochemistry, arousal, evolution — each with its own evidence and its own weaknesses, and each best held within an interactionist frame rather than asserted as a sole cause.
Full citation: Raine, A., Buchsbaum, M. & LaCasse, L. (1997) Brain abnormalities in murderers indicated by positron emission tomography. Biological Psychiatry, 42(6), 495–508.
Raine and colleagues set out to test, using brain imaging, whether people who had committed violent murder show localised brain dysfunction compared with non-murderers — in particular, whether they show reduced activity in regions previously linked to violence and impulse control (the prefrontal cortex) and abnormal activity in subcortical, limbic structures (amygdala, hippocampus, thalamus). The study aimed to provide direct evidence for a brain basis of violent behaviour, distinct from the indirect inferences of earlier work.
The study used an experimental, quasi-experimental design with two groups compared on brain-activity measures — a matched-groups (independent measures) comparison.
Participants were free of medication for two weeks before scanning, and none had a history that would confound the brain measure beyond the matched variables.
Each participant was injected with a radioactively-labelled glucose tracer (fluorodeoxyglucose) and then performed a continuous performance task (CPT) — a target-detection task requiring sustained attention — for around 32 minutes. The CPT is designed to activate the frontal regions of interest, so that differences in activity reflect functioning under cognitive demand rather than at rest. After the uptake period, participants were PET-scanned (positron emission tomography), which measures the rate of glucose metabolism in different brain regions — a proxy for how hard each region is working. The researchers compared the two groups' relative glucose metabolism across a series of predefined cortical and subcortical regions.
Why the CPT matters for evaluation. Because the task engaged the prefrontal cortex, the study measured brain function during controlled cognitive activity, giving it more validity than a resting scan. But it also means the findings are about the brain doing this particular task, and the study is correlational: it shows an association between being a violent offender and a pattern of brain activity, not that the brain pattern caused the violence.
Compared with controls, the murderers (NGRIs) showed a distinctive pattern:
Reading the findings carefully. A common error is to describe the murderers as having "damaged" or "broken" brains. The study reported differences in metabolic activity during a specific task, not lesions or structural damage, and the differences were relative to a matched control group, not absolute abnormalities. It is also important that the pattern was not uniform across the whole brain: the very fact that several regions showed no difference is part of what makes the localised interpretation credible, and it guards against the lazy conclusion that these individuals were simply "abnormal all over". Precision about what was and was not found is itself an AO1 discriminator and protects against over-claiming in evaluation.
Raine and colleagues concluded that murderers pleading NGRI show brain dysfunction in regions associated with violence — reduced prefrontal functioning (linked to loss of impulse control, poor decision-making and failure to inhibit aggression) and abnormal subcortical/limbic activity (linked to abnormal emotional responses and heightened aggression). They were, however, careful and explicit about the limits: the findings do not demonstrate that violence is caused by biology alone; they do not show these brain differences cause violence; they cannot be generalised to all types of offender (only to this specific violent, NGRI group); and brain dysfunction is only one predisposing factor among many, interacting with social and psychological influences.
| Strength | Limitation |
|---|---|
| Objective, scientific measure (PET metabolism) with a well-matched control group, including schizophrenia-matched controls to remove that confound | Correlational: shows an association, not that brain abnormality causes violence — reverse or third-variable explanations remain |
| Task-based (CPT) rather than resting, so it captures brain function under cognitive demand | Highly specific, unrepresentative sample (murderers pleading NGRI in California) — poor generalisability to other offenders or the wider population |
| Localised differences (some regions differed, others did not) support a specific rather than global claim | PET is an indirect proxy for brain activity with limited spatial/temporal resolution by modern standards |
| Practical and theoretical value: informs the biology of violence and debates about responsibility | Socially sensitive and open to misuse — a "violent brain" claim could be used to stigmatise, screen or excuse |
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