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Biological explanations of offending propose that criminal behaviour is, at least in part, the product of innate biological factors — the body and brain an individual is born with — rather than solely the product of social or environmental influence. The AQA specification requires three strands: a historical explanation (Lombroso's atavistic form), genetic explanations (twin and adoption studies, and candidate genes), and neural explanations (the role of the prefrontal cortex, of conditions such as antisocial personality disorder, and the proposed role of mirror neurons). Together these strands locate at least some of the causes of offending in genes, brain structure and neurochemistry. Engaging with them seriously also means engaging with two of the deepest debates in psychology — the nature–nurture debate and the issue of biological determinism — because if offending has biological roots, difficult questions arise about responsibility, free will and how society should respond. Throughout, offending is examined strictly as a scientific phenomenon.
Key Definition: Biological determinism is the view that behaviour is governed by biological factors (genes, brain structure, hormones, neurochemistry), such that individuals have limited free will over their actions.
This lesson addresses the following point from the AQA A-Level Psychology (7182) specification, Paper 3, Section D — Forensic Psychology:
It develops the named content — Lombroso's atavistic form; genetic explanations including twin studies, adoption studies and candidate genes (MAOA, CDH13); and neural explanations including the prefrontal cortex, antisocial personality disorder and mirror neurons — and prepares you to describe (AO1) and evaluate (AO3) these explanations, including in relation to the nature–nurture debate and biological determinism. Questions on this topic are usually split AO1/AO3 only, with no AO2 application unless a scenario stem is provided; this lesson notes where that applies.
Cesare Lombroso, an Italian physician, is regarded as the founder of criminal anthropology and of a biological criminology. In L'Uomo Delinquente ("Criminal Man," 1876) he proposed that criminals are evolutionary throwbacks (atavisms) — individuals who have not fully evolved and who therefore retain primitive physical and psychological traits that predispose them to offend. On this view the "born criminal" is a distinct biological sub-type, lacking the evolutionary development that allows others to adjust to the demands of civilised society. Lombroso's claim was therefore both biological and deterministic: such individuals were, in his framing, unable to conform.
Lombroso held that born criminals could be recognised by physical features (stigmata) resembling those of earlier evolutionary ancestors:
He examined the skulls and physical features of large numbers of convicted criminals (and used living soldiers as a comparison group), concluding that a substantial proportion of offenders displayed atavistic characteristics, and that specific crimes were associated with specific features — for instance he linked particular facial and bodily traits to particular categories of offending. He later refined his position to acknowledge other categories of criminal (such as the "insane" criminal and the "occasional" criminal influenced by circumstance), conceding that not all offending was atavistic.
Although the theory is wholly rejected today, it occupies an important place in the history of forensic psychology and is examined for what it reveals about the development of scientific criminology. Before Lombroso, crime was understood largely through the lens of free will, sin and morality: the offender was a rational agent who had chosen evil. By insisting that offending might have natural, bodily causes that could be measured and compared, Lombroso helped to inaugurate a positivist criminology — the idea that crime is a phenomenon to be studied with the methods of natural science. In this respect, despite the falsity of his specific claims, he is a genuine precursor of the modern genetic and neural explanations that follow, which pursue the same basic intuition (that biology contributes to offending) with vastly more rigorous methods. The contrast between Lombroso's flawed attempt and contemporary work is itself instructive: it shows that taking a biological stance is not enough; the explanation must also be falsifiable, properly controlled and free of the social prejudices that distorted his interpretations.
| Contribution | Serious limitation |
|---|---|
| Lombroso was among the first to study crime empirically — using measurement and a comparison group — shifting criminology from moral and religious explanation towards scientific investigation | He did not control for confounding variables: poverty, poor nutrition and disease could plausibly produce both the physical features he recorded and a greater likelihood of conviction |
| He moved the focus from punishment towards understanding the causes of crime, helping to found a more humane, treatment-oriented criminology | His ideas were appropriated to justify racist and eugenic programmes; describing offenders as primitive "throwbacks" with distinct appearances lent spurious authority to discrimination |
| His insistence that offending has natural causes anticipated later, better-evidenced biological work | The theory is biologically reductionist, collapsing complex behaviour into physical appearance and ignoring social and psychological factors |
| Goring (1913) compared around 3,000 English convicts with non-criminal controls and found no distinct set of physical features marking out criminals, directly undermining the central claim |
Modern biological explanations focus on genes as a source of predisposition to offending. The guiding question is whether crime runs in families because relatives share genes, because they share an environment, or — as is most likely — because the two interact.
It is worth being clear at the outset about what could be inherited. No serious researcher claims there is a gene "for" burglary or fraud, because crime is a legal and social category, not a biological trait, and what counts as a crime varies across time and place. What might be heritable are underlying dispositions that raise the probability of offending — for example a temperament marked by high impulsivity and sensation-seeking, low autonomic arousal that makes punishment less effective, or deficits in the empathy and impulse-control systems. On this view genes act distally: they shape a nervous system that, in certain environments, makes antisocial behaviour more likely. This framing matters for evaluation, because it explains both why genetic effects on "crime" are real but modest, and why they are so heavily conditioned by environment.
Twin studies exploit the fact that monozygotic (MZ, "identical") twins share effectively 100% of their genes while dizygotic (DZ, "fraternal") twins share on average about 50%, like ordinary siblings. If a behaviour is genetically influenced, MZ twins should show higher concordance (both twins offending) than DZ twins. Christiansen (1977) examined a sample drawn from the Danish Twin Register (in the region of 3,500 twin pairs) and reported concordance for criminal convictions of approximately 35% in MZ twins versus about 13% in DZ twins. Conclusion: the markedly higher MZ concordance points to a genetic contribution to offending — but, crucially, because MZ concordance falls well short of 100%, genes cannot be the whole story, and the environment must also matter substantially.
The logic of the twin method deserves emphasis because it is frequently tested. The design holds genetic similarity as the variable that differs between MZ and DZ pairs, while attempting to hold environment roughly constant (both members of a twin pair are typically raised together). If concordance is higher for the genetically more similar (MZ) pairs, the difference is attributed to genes. The strength of the method is that it provides a natural experiment that would be impossible to engineer; its much-discussed weakness, examined in the evaluation, is the equal-environments assumption — the questionable premise that MZ and DZ pairs share equally similar environments. An earlier, smaller twin study by Lange (1929) had reported a far more dramatic difference (with most MZ but few DZ pairs concordant for imprisonment), but its tiny sample and crude methods make Christiansen's much larger, register-based study the more trustworthy estimate.
Adoption studies separate genetic from environmental influence more cleanly, because the adoptee is raised apart from their biological relatives. Mednick et al. (1984) examined a very large Danish cohort (over 14,000 adoptees), comparing adoptees' convictions against the convictions of their biological parents (genetic influence) and their adoptive parents (environmental influence):
| Biological parent convicted | Adoptive parent convicted | Adoptee convicted |
|---|---|---|
| No | No | 13.5% |
| No | Yes | 14.7% |
| Yes | No | 20.0% |
| Yes | Yes | 24.5% |
Conclusion: having a convicted biological parent predicted the adoptee's offending more strongly than having a convicted adoptive parent, supporting a genetic influence. However, the highest rate occurred when both biological and adoptive parents were convicted (24.5%), which is exactly the signature of a gene–environment interaction rather than pure genetic determination.
Adoption studies are valued precisely because they go some way towards unconfounding genes and environment: the adoptee carries the biological parents' genes but is raised in the adoptive parents' environment, so a stronger association with biological-parent criminality is hard to attribute to shared upbringing. Two cautions nonetheless apply. First, selective placement can blunt the separation, because adoption agencies have historically tended to place children in homes broadly resembling the biological background, partially re-correlating genes and environment. Second, adoption is rarely instantaneous, so an adoptee may have spent formative early months or years with the biological mother before placement, leaving room for prenatal and early-environmental influence. These do not overturn the genetic signal, but they reinforce the conclusion that the data describe an interaction rather than pure heredity.
Rather than a single "criminal gene," research points to particular candidate genes that may raise the risk of violent offending in interaction with the environment. The most-discussed is MAOA, which codes for the enzyme monoamine oxidase A that metabolises (breaks down) neurotransmitters including serotonin, dopamine and noradrenaline. A low-activity variant has been associated with aggression, and the gene is sometimes informally called the "warrior gene." CDH13, involved in neural connectivity and impulse control, has also been implicated. Tiihonen et al. (2015) analysed a large Finnish prison sample and reported that low-activity MAOA together with CDH13 variation was associated with extremely violent offending; they estimated that a notable share of violent crime in their sample was statistically attributable to these variants. Conclusion: specific genotypes may contribute to a predisposition to violence — though, as the evaluation stresses, such genes confer risk, not destiny.
Note on XYY: an older hypothesis linked an extra Y chromosome (the XYY karyotype) in males to violent offending. Witkin et al. (1976), studying a large Danish sample, found that any excess offending among XYY men was largely explained by lower intelligence rather than heightened aggression, and the supposed XYY–violence link is now largely discredited. The episode is a useful caution against leaping from a chromosomal anomaly to a behavioural conclusion.
Neural explanations locate offending in the structure and function of the brain, particularly in the systems governing impulse control, emotion and empathy.
The prefrontal cortex (PFC) supports executive functions including planning, impulse control, decision-making and the regulation of aggression; damage or dysfunction here is associated with disinhibited, impulsive and aggressive behaviour. Raine, Buchsbaum and LaCasse (1997) used PET scans to compare 41 individuals charged with murder (who had pleaded not guilty by reason of insanity) with 41 matched controls. Findings: the offender group showed reduced activity in the prefrontal cortex, together with abnormal activity in the amygdala (emotional processing, fear), and atypical functioning in the hippocampus and thalamus. Conclusion: violent offending is associated with dysfunction in brain regions responsible for controlling impulses and processing emotion. Raine was explicit that this is an association, not a demonstrated cause — the data do not show that anyone was "born to kill."
Much offending, particularly persistent and violent offending, is associated with antisocial personality disorder (APD) — a condition characterised by impulsivity, a lack of empathy and guilt, and a disregard for others' rights and for social norms. Neural research links APD to reduced activity and atypical structure in prefrontal regions and the limbic system, consistent with the impulse-control and emotion-processing deficits seen in Raine et al. Some evidence also points to differences in the autonomic nervous system (for example, low resting arousal), which may make such individuals less responsive to the threat of punishment and harder to socialise through conditioning — a point that connects directly to Eysenck's account in the psychological-explanations lesson.
A more recent proposal concerns mirror neurons — cells that fire both when an individual performs an action and when they observe another performing it, and which are implicated in empathy by allowing us to "mirror" others' emotional states. Research suggests that individuals with APD are not entirely without empathy but may show reduced or intermittent mirror-neuron activity: when explicitly asked to empathise, their mirror systems can activate relatively normally, but the system does not engage automatically in the way it does for most people. Conclusion: rather than a permanent absence of empathy, APD may involve an empathy "switch" that is off by default, offering a neural account of how offenders can harm others without the inhibiting emotional response empathy normally provides. This is theoretically important because it reframes the empathy deficit in APD as a problem of automatic engagement rather than total capacity, which has implications for treatment: if the empathic response can be deliberately switched on, then interventions that train offenders to take the victim's perspective might, in principle, recruit a system that is present but dormant.
Neural explanations also encompass neurochemistry. Low levels of the neurotransmitter serotonin are associated with reduced impulse control and an increased propensity for impulsive aggression, because serotonin normally exerts an inhibitory, regulating influence over behaviour; this connects directly to the MAOA findings, since the MAOA enzyme metabolises serotonin and a low-activity variant disturbs its regulation. The hormone testosterone has also been linked to aggression, with some studies reporting higher levels in violent offenders, although the relationship is complex and bidirectional (behaviour and social context can influence hormone levels, not only the reverse). These neurochemical strands reinforce the broader neural picture — that offending, particularly impulsive and violent offending, is associated with atypical functioning in the systems that normally restrain aggression — while also illustrating how difficult it is to establish the direction of causation.
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