4.3.9 - Biological explanations of offending behaviour

The Biological Scope

This lesson covers the updated AQA requirement: biological explanations of offending behaviour: genetics and neural explanations. The two required routes are:

Biological explanations should be written as risk explanations, not as "crime genes" or "criminal brains". Most people with a biological risk factor do not offend, and many offenders do not have the same biological profile. For AQA, the strongest answer says that biology may help explain vulnerability, especially when combined with environmental factors such as maltreatment, peer influence, poverty, substance use or opportunity.

There are two scope traps to avoid. First, do not turn this lesson into the neighbouring lesson on psychological explanations such as Eysenck, cognitive distortions or differential association theory. Second, do not make the old historical atavistic-form approach the centre of the answer. For this updated 2025 point, the focus is genetics and neural explanations.

Genetic Evidence

Genetic studies compare patterns of similarity between people with different degrees of genetic relatedness.

Genetic explanations begin with family resemblance. If offending has a genetic component, people who are more genetically similar should show more similar patterns of antisocial or criminal behaviour. Two useful research designs are twin studies and adoption studies.

Twin Evidence

Rhee and Waldman (2002) conducted a meta-analysis of 51 twin and adoption studies of antisocial behaviour. Their best-fitting model estimated genetic influence at about 41% in total: additive genetic influence of .32 and non-additive genetic influence of .09. Shared environmental influence was estimated at .16, and non-shared environmental influence at .43.

What this suggests: genetic factors make a meaningful contribution to antisocial behaviour, but environmental influences are also substantial.

Kendler et al. (2015) used the Swedish Twin Registry and Swedish Crime Register to study 21,603 twin pairs. For all criminal convictions, heritability was estimated at about 45% in both sexes. Shared environment still mattered, accounting for 18% of variance in liability for females and 27% for males.

Interpreting the evidence: this is strong evidence because it uses a large national register rather than a small volunteer sample. Twin comparisons nevertheless assume that relevant environments are sufficiently comparable: MZ twins may be treated more similarly than DZ twins, so greater MZ resemblance is not automatically genetic. However, official convictions are not the same as all offending. They are affected by detection, policing, prosecution and social inequality.

Reading genetic evidence

Imagine a study finds that identical twins are more similar in conviction records than non-identical twins. This fits genetic influence because the first group shares more genetic variation. It is not enough simply to say “both twins offended”: both groups may also share upbringing, and similarity must be compared. Even a substantial heritability estimate is not a probability that a particular child will offend. A group estimate of 45% does not mean genes caused 45% of one person's offence, and it does not imply that prevention is ineffective. Changing environments can change outcomes even for a heritable trait.

Adoption Evidence

Mednick, Gabrielli and Hutchings (1984) compared court convictions for 14,427 adoptees with the convictions of their biological and adoptive parents. They found a significant association between adoptees and biological parents for property-crime convictions, but not for violent crimes. They did not find a significant association between adoptees and adoptive parents' convictions. Siblings adopted into separate homes also tended to be concordant for convictions, especially when their shared biological father had a conviction record.

What this suggests: the adoption evidence supports a genetic influence because the link was stronger with biological parents than adoptive parents.

Interpreting the evidence: Adoption separates some shared upbringing from shared inheritance, but prenatal influences, early contact and selective placement with similar families can still confound the comparison. Mednick et al.'s finding was clearer for property crime than violent crime. A careful answer should not use it as proof that genes explain every type of offending.

Worked application: If Malik was adopted as a baby and later receives a conviction, and records show that his biological father also had convictions, a genetic explanation would say Malik may have inherited a vulnerability. It would not say Malik inherited "crime" itself. His adoptive environment, peers, opportunities, school experience and choices would still matter.

Candidate Genes And Interaction

Candidate-gene studies investigate possible biological mechanisms while testing how inherited differences interact with experience.

Candidate-gene research asks whether particular genes are associated with aggression, impulsivity or serious offending. The exam danger is to write as if one gene "causes crime". Modern genetic evidence does not support that. Candidate genes are better understood as part of a wider vulnerability system.

MAOA And Maltreatment

Caspi et al. (2002) studied males from birth into adulthood and examined whether MAOA genotype moderated the effect of childhood maltreatment. They found that maltreated males with a genotype linked to higher MAOA activity were less likely to develop antisocial problems than maltreated males with lower-activity MAOA. The key point is the interaction: maltreatment predicted antisocial behaviour more strongly for some genotypes than others.

To recognise an interaction, compare the effect of the environment across genotypes: does maltreatment predict the same increase in problems in each group? If the increase differs, the environmental effect depends on genotype. Simply observing both a genetic variant and maltreatment in one person cannot demonstrate this statistical pattern. Because maltreatment was not randomly assigned, the study also cannot rule out every alternative explanation.

Caspi et al. are useful because they move the argument beyond nature versus nurture. The research suggests that some genetic profiles may increase sensitivity to adverse environments, while supportive environments may reduce the likelihood that vulnerability develops into offending.

MAOA, CDH13 And Extreme Violence

Tiihonen et al. (2015) studied two cohorts of Finnish prisoners. They reported that a low-activity MAOA genotype and variation in CDH13 were associated with extremely violent behaviour, defined as at least ten committed homicides, attempted homicides or batteries. The researchers found no substantial signal for these genes among non-violent offenders, and reported a population-attributable estimate of 5–10% of severe violent crime in Finland under their model. That estimate relies on assumptions about the association; it is not a proportion of violence experimentally shown to be caused by these variants.

What this suggests: candidate-gene research suggests possible genetic contributions to vulnerability. These associations require replication; they are not a genetic test that can identify future offenders.

Interpreting the evidence: even in Tiihonen et al., the estimate was 5-10% of severe violent crime, not most crime. The findings relate to extreme Finnish violent offending, so they should not be generalised casually to all offenders, all countries or all types of crime.

Best exam wording: "genes may predispose individuals to traits such as impulsivity, poor emotional regulation or reduced fear learning, which may increase the probability of offending in certain environments."