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Biological explanations of criminality propose that offending is, at least in part, the product of innate biological factors — the brain, genes and inherited temperament an individual is born with — rather than solely the product of social experience. Where social explanations (covered in the next lesson) emphasise learning and environment, biological explanations locate some of the causes of offending in neural structure and function, in genetic predisposition, and in personality dimensions that are themselves biologically grounded. This lesson examines three strands the Edexcel specification treats as central: brain and neural explanations (particularly prefrontal cortex dysfunction and the role of specific brain regions in impulse control and emotion), genetic explanations (twin and adoption studies, and candidate genes such as MAOA), and Eysenck's criminal personality theory (extraversion, neuroticism and psychoticism and their biological basis). Engaging seriously with these explanations also means engaging with two of the deepest debates in psychology — nature versus nurture and 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 biological explanations of criminal behaviour content of Edexcel 9PS0 — Paper 2, Topic 6: Criminological Psychology — specifically brain/neural explanations, genetic explanations, and the personality (Eysenck) explanation, together with their evaluation.
Connects to…
Neural explanations locate offending in the structure and function of the brain, particularly in the systems governing impulse control, emotion and empathy. The guiding idea is that atypical functioning in these systems can disinhibit aggression and reduce the emotional restraints that ordinarily prevent people harming others.
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 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 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 personality account below.
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 below, since the MAOA enzyme metabolises serotonin. The hormone testosterone has also been linked to aggression, though the relationship is complex and bidirectional (behaviour and social context can influence hormone levels, not only the reverse). These 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 illustrating how difficult it is to establish the direction of causation.
Genetic explanations propose that a predisposition to offending can be inherited. 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 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 — 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. 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.
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. 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.
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. Brunner et al. (1993) studied a large Dutch family in which many of the men showed a pattern of impulsive aggression and violent offending; the affected men were found to have a rare mutation causing a deficiency of MAOA, disrupting the metabolism of these neurotransmitters. A low-activity variant of the gene has since been associated with aggression, and it is sometimes informally called the "warrior gene." Conclusion: specific genotypes may contribute to a predisposition to violence — though, as the evaluation stresses, such genes confer risk, not destiny, and the famous finding in this literature is that low-activity MAOA appears to raise risk mainly in individuals who also experienced childhood maltreatment.
graph TD
A[Biological Explanations of Criminality] --> B[Brain / Neural]
A --> C[Genetic]
A --> D[Personality: Eysenck]
B --> B1[Prefrontal cortex: Raine et al. 1997]
B --> B2[Amygdala / limbic system / APD]
B --> B3[Serotonin & testosterone]
C --> C1[Twin studies: Christiansen 1977]
C --> C2[Adoption studies: Mednick et al. 1984]
C --> C3[Candidate gene MAOA: Brunner et al. 1993]
D --> D1[Extraversion / Neuroticism / Psychoticism]
D --> D2[Poor conditioning of conscience]
Hans Eysenck (1964) proposed that criminal behaviour can be explained by personality type, itself rooted in biological predisposition and shaped through socialisation. Using factor analysis, Eysenck identified dimensions of personality measured by the Eysenck Personality Questionnaire (EPQ). Because these dimensions are held to be biologically based and largely inherited, Eysenck's theory sits within the biological family of explanations even though it also invokes learning.
| Dimension | Description | Proposed biological basis |
|---|---|---|
| Extraversion (E) | Sociable, sensation-seeking, impulsive | Chronically low cortical arousal, so the person seeks stimulation to reach an optimal level |
| Neuroticism (N) | Anxious, moody, emotionally unstable, over-reactive | A highly reactive autonomic nervous system, producing strong, rapid fight-or-flight responses |
| Psychoticism (P) | Cold, aggressive, impulsive, lacking empathy, egocentric | Associated with higher testosterone and dysregulated neurotransmitters |
Eysenck argued that the typical offender scores high on all three dimensions (high E, high N, high P):
Crucially, Eysenck linked personality to conscience via learning. He argued that socialisation is a process of classical (and operant) conditioning: in normal development, children repeatedly experience anxiety when antisocial impulses are punished, until the mere anticipation of wrongdoing triggers a conditioned anxiety response that functions as a conscience and inhibits offending. People high in extraversion (and high in neuroticism) condition poorly — extraverts because their under-arousal makes the punishing stimulus less impactful, neurotics because their high baseline anxiety interferes with learning the specific association. The result is a weak conditioned conscience and a greater readiness to offend. This is the theory's distinctive move: it ties a biological trait to a learning deficit to a behavioural outcome.
graph TD
A[High Extraversion] --> B[Low Cortical Arousal]
B --> C[Poor Conditionability]
C --> D[Weak Conscience Development]
D --> E[Failure to Internalise Social Norms]
E --> F[Offending Behaviour]
G[High Neuroticism] --> H[Emotional Instability / High Anxiety]
H --> C
I[High Psychoticism] --> J[Lack of Empathy / Aggression]
J --> F
Eysenck and Eysenck (1977) compared the EPQ scores of male prisoners with controls and found prisoners scored higher on P and N. Support for the E dimension, however, has been inconsistent across studies — a serious problem given that E is central to the conditioning mechanism. Some researchers have suggested that the two components of extraversion (sociability and impulsivity) should be separated, with only the impulsivity component reliably linked to offending. It is worth noting how the theory blends nature and nurture: the personality dimensions are biologically based and largely inherited, but whether a given temperament leads to offending depends on socialisation — specifically on whether conditioning successfully installs a conscience. In this sense Eysenck's theory is already implicitly interactionist, which is a strength to acknowledge in evaluation.
Note: The strongest single evaluative point on Eysenck is the weak and inconsistent evidence for the E dimension, since E carries the theory's causal mechanism (poor conditioning). Most reliable support is for P and N.
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