Biological Theories of Crime

Biological theories of crime argue that whether someone offends depends partly on their biological nature: genetic, hormonal, or neurological factors present at birth or acquired later.

No one is a ‘born criminal,’ because crime itself is a social and legal category, not a fixed biological one. Instead, these theories try to link general traits such as aggression, impulsivity, and risk-taking to whichever behaviors a given society happens to criminalize.

History and Overview

Biological criminology traces back to 19th-century Italy, and its early history includes a documented, disastrous political misuse that is worth understanding on its own terms.

Lombroso, Phrenology, and Early Biological Criminology

Forensic biology first became a science in its own right in 19th-century Italy, with the physician Cesare Lombroso as its founding father.

Lombroso developed the idea of the “born criminal” from two influences: phrenology, the discredited study of skull shape as a guide to character, and Darwin’s theory of evolution.

Lombroso was not working in isolation. He drew on the French crime statisticians André-Michel Guerry and Adolphe Quetelet.

Their data, linking age, gender, social origin, and crime, pointed toward environmental and social causes as well as biological ones. The pattern was striking.

His students leaned further into this hypothesis, producing the integrated biosocial theories that dominate the field today. Biosocial theories treat biology and environment as interacting causes of crime, rather than as rival explanations.

Lombroso’s ideas travelled fast. In the German-speaking world, the psychiatrist Emil Kraepelin promoted a parallel “degeneration thesis.”

It held that criminals pathologically and hereditarily deviated from a normal genetic type, identifiable by psychological rather than physical traits.

Eugenics and the Nazi Misuse of Biological Theory

This lineage had a darker, documented history.

Both the Weimar Republic and the Third Reich drew on these theories to justify so-called “racial hygiene” programs. They branded entire ethnic minorities as genetically criminal and inferior.

German legal scholars such as Franz Exner and Edmund Mezger cited the twin studies of Johannes Lange and the genealogical research of Friedrich Stumpfl as scientific justification. Both argued that criminality could be explained by genetic predisposition alone.

The Nazi party separately drew on the psychiatrist Ernst Kretschmer’s constitutional theory, which held that physiological abnormalities of the brain, skull, or body structure could produce crime.

The consequences were catastrophic.

Because of these consequences, biological theories of crime largely lost scientific standing after the Second World War.

Most criminal biologists since have abandoned the idea that offending can be explained by biology alone, preferring approaches that combine biology and environment. Terrie Moffitt’s Two-Path theory, discussed next, is a leading modern example.

Degeneration Theory (1857)

Degeneracy Theory, an offshoot of 19th-century research into biological theories of crime, argues that certain lower social classes and races were predisposed to neurological and mental illness by inheritance. This, the theory claimed, made them more likely to commit crimes.

Those of low social standing — prostitutes, criminals, the poor, and those with mental illness — were considered morally defective. They were said to represent a regression in human evolution.

B.A. Morel (1857) proposed the first theory of progressive degeneracy in his book, Traits des Dégénérescences Physiques, Intellectuelles et Morales de l’Espèce Humaine.

Morel believed that using substances such as hashish, alcohol, and opium caused progressive physical and moral deterioration.

The claim was radical.

He argued this deterioration would pass from one generation to the next, worsening a society’s intellectual and moral character over time.

This theory would come to influence Cesare Lombroso’s biological theory of crime.

That claim mattered most.

Another key claim of degeneration theory is that moral degeneracy itself is heritable.

Degeneration theorists widely believed that the moral and physical pathologies behind low social status would persist and spread from generation to generation, both biologically and socially.

Thus, degeneration theorists believed that the so-called “miscegenation” between morally defective people should be regulated by eugenics and moral hygiene for the good of society.

Atavistic Theory of Crime (1876)

The Born Criminal as an Evolutionary ‘Throwback’

Cesare Lombroso (1876) was most famous for developing the atavistic theory of crime in his book, The Criminal Man. In this book, Lombroso argued that there is a distinct biological class of people prone to criminality.

Lombroso’s (1876) theory of criminology suggests that criminality is inherited and that someone “born criminal” could be identified by the way they look. These people exhibited ‘atavistic’ (that is, primitive) features.

Lombroso suggested that they were ‘throwbacks’ who had biological characteristics from an earlier stage of human development that manifested as a tendency to commit crimes.

Credit: Wellcome Library, London. Wellcome Images images@wellcome.ac.uk http://wellcomeimages.org Six figures illustrating types of criminals Printed text L’Homme Criminel Lombroso, Cesar Published: 1888

Lombroso’s Physical ‘Types’ of Criminals

Lombroso claimed that criminal types were visibly distinguishable from the general population.

• Thieves: expressive faces, manual dexterity, and small, wandering eyes.
• Murderers: cold, glassy stares, bloodshot eyes, and hawk-like noses.
• Sex offenders: thick lips and protruding ears.
• Female criminals: shorter, more wrinkly, with darker hair and smaller crimes than normal women.

This meant, Lombroso argued, that criminals were at a more primitive stage of evolution than non-offenders, making them unable to fit into contemporary society and thus prone to committing crimes. This came with the implication that criminality was heritable.

Sheldon’s Somatotype Theory (1942)

William Sheldon (1942) proposed a strong correlation between personality and somatotype (i.e., physique).

From a study of several hundred male physiques, he derived three body types:

1. The ectomorph, characterized by a thin, wiry frame.
2. The endomorph, heavy and rounded.
3. The mesomorph, with a solid, muscular frame.

Each body type was associated with a particular personality:

1. Ectomorph = introvert, quiet, fragile, sensitive
2. Endomorph = relaxed, sociable, tolerant, peaceful
3. Mesomorph = aggressive, assertive, and adventurous.

Sheldon noted that the vast majority of criminals were mesomorphs. One explanation for this is that a solid, muscular person becomes involved in crime at an early age due to their intimidating appearance.

This biological theory may seem implausible, but people often stereotype others on characteristics such as their appearance.

Certain individuals (e.g., the police) may make “snapshot” judgments about people, which may have implications for criminal behavior.

Terrie Moffit’s Two-Path Theory (1993)

Terrie Moffit’s Two-Path theory is a biosocial theory of crime.

Moffitt (1993) proposed two groups of offenders. Life-course-persistent offenders show anti-social, criminal behavior that begins in childhood and continues to worsen thereafter. Adolescence-limited offenders, by contrast, show antisocial behavior that begins in adolescence but ends in young adulthood.

While life-course-persistent offenders are rare but pathological in nature, adolescent-limited offenders are relatively common, temporary, and near the normal.

The two paths differ sharply.

Moffitt’s two-path theory has had important implications for criminal policy as one of the most widely received modern criminological theories.

Notably, those who follow Moffit’s theory believe that about 5% of the population could be life-course-persistent offenders.

The government of Hamburg, Germany, in response to this theory, has screened primary-school-age children in an attempt to provide social therapeutic measures that could possibly compensate for poor parental support.

Modern Biological Theories of Crime

Modern biological theories of crime focus specifically on how different regions of the brain are responsible for thoughts, emotions, and behaviors, and how the dysfunction of these regions can cause criminality (Raine, 2008; Viding et al., 2005; Newsome, 2014).

Neurological Theories of Crime

Neural explanations look at the structure and functioning of the central nervous system, and criminologists have focused especially on the frontal lobe.

The frontal lobe is involved in abstract thought, planning, goal formation, sustaining attention, self-monitoring, and behavioral inhibition (Moffitt, 1990; Raine, 2002).

The evidence here is consistent.

The pattern holds across methods.

Neuroscientists also study how neurotransmitters, chemicals in the brain, influence thought, emotion, and behavior.

Excessive dopamine, for example, has been linked to aggressive and criminal behavior, and antipsychotic drugs that reduce dopamine may also reduce aggression.

Increased norepinephrine can produce aggressive behavior, while reduced levels can lead to antisocial behavior. Both extremes, in other words, can cause problems.

Serotonin, an inhibitory neurotransmitter used throughout the brain including the limbic system and frontal cortex, is of particular interest.

Researchers have found that reduced serotonin levels are linked to criminal behavior and to the management of impulsivity (Brizer, 1988; Raine, 2008).

Genetic Explanations

Genetic explanations of crime propose that genetic factors could predispose individuals to offend. The reasoning is that genes code for physiological factors, such as the structure and functioning of the nervous system and neurochemistry.

As in early biological theories of crime, criminologists use family, adoption, and twin studies to estimate how heritable certain traits are (Plomin, 2004). The logic is simple.

In these studies, researchers compare how closely an individual’s behavior resembles their biological relatives versus their adoptive ones. The more it resembles biological relatives, the more genetic the trait is judged to be.

The design was elegant.

Rhee and Waldman (2002) reviewed twin and adoption studies and found substantial genetic and environmental influences on antisocial behavior.

Specifically, they found that additive genetic effects explained about 32% of the variation in antisocial behavior.

Nonadditive genetic effects explained a further 9 percent, shared environment 16%, and unique, non-shared environment the remaining 43%.

The picture was mixed.

After Rhee and Waldman, Moffitt (2005) reviewed the field again and concluded that genetic influence accounts for about half of the population’s variation in antisocial behavior.

Gene-Environment Interactions

People with different genetic make-ups are likely to respond differently to the same environment.

Those with a genetic predisposition toward criminality are more likely to offend if exposed to a criminogenic environment.

Those without such a predisposition are unlikely to offend even in that same environment.

The gene alone is not enough.

Caspi et al. (2002) found direct evidence of this interaction.

They studied a gene that produces an enzyme breaking down neurotransmitters such as serotonin and dopamine.

On its own, this genetic variant had no direct effect on behavior.

Context changed everything.

However, boys who were maltreated as children and who also carried the low-activity version of the gene were far more likely to develop antisocial behavior problems.

The gene mattered only in combination with adversity (Kim-Cohen et al., 2006; Caspi et al., 2002).

Critical Evaluation

The biological approach to crime faces real limitations, on both scientific and ethical grounds.

1. Limited by Methodology: Genetic studies cannot yet pinpoint which specific genes cause behavioral differences, and even careful twin and adoption studies can inflate the apparent genetic contribution.
2. Socially and Ethically Sensitive: If offending has a genetic basis, questions arise about responsibility and testing, the same reasoning that once produced the eugenic programs described above.
3. Findings Often Fail to Replicate: Many single-study candidate-gene findings, like the original MAOA result, later replicated only at a much smaller effect size once pooled.
4. Measures Convictions, Not Offending: Studies relying on criminal convictions test who gets caught, not who actually offends, since most crime goes officially unrecorded.

Limited by Methodology

Genetic studies of crime cannot, by themselves, determine which specific genetic factors lead to behavioral differences.

Many genes can disrupt normal development in ways that produce abnormal behavior.

Two gene families dominate this research.

Criminologists have been especially interested in two types of genes: those that control dopamine and those that control serotonin.

Variants in the genes that control dopamine have been linked to serious and violent antisocial behavior (Comings et al., 2000).

Low levels of serotonin, separately, have been linked to increases in antisocial behavior (Raine, 2008).

These specific-gene findings illustrate the wider problem.

Walters and White’s (1989) review, pointedly titled “Heredity and crime: bad genes or bad research?,” re-examined the twin and adoption studies available at the time.

They found problems that could inflate apparent heritability, including unrepresentative samples, inconsistent definitions of criminality, and early twin studies that assumed rather than verified zygosity.

Their verdict was cautious.

They concluded the genetic contribution was probably real, but likely overstated.

Later, more rigorous meta-analyses using verified zygosity have continued to find a genetic contribution, absorbing this methodological caution rather than being refuted by it.

Socially and Ethically Sensitive

The biological approach is socially sensitive because it carries direct consequences for the legal system and society as a whole.

If offending has a genetic or neurological basis, questions arise about how far offenders should be held personally responsible for their crimes.

A further question follows.

What should be done with individuals identified as carrying a predisposing biological profile?

Crime-prevention logic could, in principle, extend to genetic testing of the public.

These are not abstract worries.

The same reasoning, applied without restraint, produced the eugenic “racial hygiene” programs described above.

The XYY “supermale” episode is a further warning.

A real but modest and poorly understood biological association can harden into a stigmatizing myth once it reaches public discourse.

Behavioral geneticists now face a related, practical version of the same problem: communicating small, probabilistic risk information to families without sliding into either fatalism or determinism.

Findings Often Fail to Replicate

A second, more purely scientific limitation concerns replication.

The candidate-gene era of criminological genetics produced many single-study findings that later failed to replicate cleanly.

The MAOA-by-maltreatment finding is the best-known example.

Byrd and Manuck (2014) tested this directly, pooling the available studies on the MAOA-by-maltreatment interaction in a meta-analysis.

They found a significant, if modest, interaction effect consistent with the original pattern.

The pooled effect size, however, was smaller than several individual studies, including the original, had reported.

Independent confirmation followed.

A closely related meta-analysis of MAOA and maltreatment in predicting children’s mental health difficulties (Kim-Cohen et al., 2006) reached a consistent conclusion using an independent set of cohorts.

That independent confirmation matters.

This is not a problem unique to crime genetics; the same pattern affected candidate-gene psychiatric genetics broadly.

It is a central reason the field has shifted toward the genome-wide designs discussed next.

Measures Convictions, Not Offending

A related measurement problem compounds the interpretive difficulty throughout this literature.

Official crime statistics substantially undercount real offending, a gap criminology calls the dark figure of crime.

This gap matters.

Biological studies that rely on convictions or arrests as their outcome measure are testing correlates of getting caught and processed, not simply of offending itself.

Mednick et al.’s 1984 adoption study and much of the twin literature necessarily work this way.

Convictions are not the same as crimes.

This matters because any biological factor that also affects detectability will appear more “criminogenic” in the data than it may actually be.

Poor impulse control is one example: it can make an offender more likely to be caught in the first place.

The measurement problem, in other words, can itself masquerade as a biological one.

Contemporary Research

Is Autonomic Underarousal a Real, Replicated Finding?

A chronically low resting heart rate is one of the most consistently replicated biological correlates of antisocial behavior.

Two theories compete to explain why.

The fearlessness hypothesis says an underaroused person is less afraid of punishment.

The stimulation-seeking hypothesis says antisocial behavior is pursued because it feels exciting.

Both are plausible.

Portnoy and Farrington (2015) tested this with an updated systematic review and meta-analysis.

The pooled sample was large: child, adolescent, and adult participants, drawn from both community and offender populations.

Low resting heart rate showed a significant, consistent link to antisocial behavior across every subgroup examined, by sex, by age, and across different measures of antisociality.

That consistency stands out.

It makes low heart rate one of the most robust biological correlates identified anywhere in this literature.

Heart rate is a marker, though, not a proven cause.

The fearlessness and stimulation-seeking explanations remain plausible interpretations rather than demonstrated mechanisms.

From Candidate Genes to the Whole Genome

The genetics of antisocial behavior has moved decisively away from single candidate genes like MAOA.

Tielbeek and colleagues (2017) ran a genome-wide association study through the Broad Antisocial Behavior Consortium.

The scale was new.

They combined data from eight cohorts and roughly 16,400 discovery participants of European ancestry.

No single gene emerged as a large, reliable driver of antisocial behavior.

Three tentative loci showed sex-specific associations.

A polygenic score built from the discovery data predicted antisocial behavior in independent Finnish samples, and antisocial behavior also shared genetic architecture with conduct problems and substance dependence.

The conclusion is that antisocial behavior is highly polygenic.

Its genetic contribution is spread across very many genes of small effect, not concentrated in one or a few “crime genes.”

Read together, these two literatures tell a coherent story.

A genuinely robust physiological correlate exists and has survived rigorous testing.

Genetic risk, meanwhile, is real but spread thinly across the genome, undercutting the old “warrior gene” framing MAOA once attracted in public discussion (Ling et al., 2019).

Evolutionary Explanations of Crime

A further strand of biological theorizing asks a different question.

Not which brain structure or gene is involved in a given act.

The question, instead, is why natural selection might have favored psychological mechanisms that, in the modern context, sometimes manifest as criminal behavior.

The logic runs backward from ordinary theory.

Evolutionary explanations do not claim that crime itself was selected for.

Crime is a socially and legally defined category with no fixed referent across evolutionary time.

Instead, the claim is narrower.

Some underlying psychological dispositions, such as status-seeking, risk-taking, jealousy, and competition for mates and resources, may have been shaped by selection pressures on ancestral populations.

These dispositions occasionally produce behavior that modern law happens to criminalize.

The Young Male Syndrome

Aim. To explain one of criminology’s most robust and cross-culturally consistent patterns: that violent and risk-taking crime is committed disproportionately by young adult men.

Method. Wilson and Daly (1985) reviewed demographic and criminological data on the age and sex distribution of violent crime across multiple societies.

They interpreted the pattern through sexual selection theory.

Results. Violent crime and dangerous risk-taking were overwhelmingly concentrated among males in their late teens to twenties.

This is the period of peak intrasexual competition for status and mates, and the pattern recurred with strikingly similar shape across very different cultures and legal systems.

Conclusion. Wilson and Daly proposed that this age-and-sex pattern reflects an evolved psychology of risk-acceptance and competitive status-seeking.

Selection, on this account, calibrated the pattern to peak when the reproductive stakes of intrasexual competition were, in ancestral environments, at their highest.

The theory explains a genuinely universal pattern that purely social explanations struggle to derive from first principles.

Its weakness is narrower.

It says comparatively little about why particular young men, rather than others of the same age and sex, actually offend.

Genetic Relatedness and the Risk of Lethal Violence

Daly and Wilson (1988) tested a related evolutionary prediction.

Parental investment theory implies people should be less willing to risk their own reproductive interests to protect a genetically unrelated child than a genetically related one.

They compared homicide statistics from multiple national records, contrasting rates of child homicide by genetic parents against rates by stepparents.

The results were striking.

Children living with a stepparent faced a substantially elevated risk of fatal abuse compared with children living with two genetic parents.

This disparity was far larger than most other known risk factors for child homicide, and it recurred across the different national datasets examined.

This is one of the most cited and broadly replicated findings in evolutionary psychology’s application to crime.

It is also one of the most contested.

Sociological critics argue the stepparent elevation may be confounded by other risk factors, such as family instability or lower household resources, rather than reflecting an evolved discrimination mechanism as such.

The raw statistical association is robust; why it exists remains a live scientific disagreement.

References

Brizer, D. A. (1988). Psychopharmacology and the management of violent patients. Psychiatric Clinics of North America, 11(4), 551-568.

Byrd, A. L., & Manuck, S. B. (2014). MAOA, childhood maltreatment, and antisocial behavior: Meta-analysis of a gene-environment interaction. Biological Psychiatry, 75(1), 9-17. https://doi.org/10.1016/j.biopsych.2013.05.004

Caspi, A., McClay, J., Moffitt, T. E., Mill, J., Martin, J., Craig, I. W., … & Poulton, R. (2002). Role of genotype in the cycle of violence in maltreated children. Science, 297(5582), 851-854.

Comings, D. E., & Blum, K. (2000). Reward deficiency syndrome: genetic aspects of behavioral disorders. Progress in brain research, 126, 325-341.

Daly, M., & Wilson, M. (1988). Evolutionary social psychology and family homicide. Science, 242(4878), 519-524. https://doi.org/10.1126/science.3175672

Kim-Cohen, J., Caspi, A., Taylor, A., Williams, B., Newcombe, R., Craig, I. W., & Moffitt, T. E. (2006). MAOA, maltreatment, and gene–environment interaction predicting children’s mental health: new evidence and a meta-analysis. Molecular psychiatry, 11(10), 903-913.

Lombroso, C. (1876). L’Uomo delinquente. Milano: Hoepli.

Lombroso, C. (2006). Criminal man. Duke University Press.

Mednick, S. A., Gabrielli, W. F., & Hutchings, B. (1984). Genetic influences in criminal convictions: Evidence from an adoption cohort. Science, 224(4651), 891-894.

Moffitt, T. (1990). The neuropsychology of juvenile delinquency: A critical review. Crime and justice, 12, 99-169.

Moffitt, T. E. (1993). Adolescence-limited and life-course-persistent antisocial behavior: A developmental taxonomy. Psychological Review, 100(4), 674-701. https://doi.org/10.1037/0033-295X.100.4.674

Moffitt, T. E. (2005). The new look of behavioral genetics in developmental psychopathology: gene-environment interplay in antisocial behaviors. Psychological Bulletin, 131(4), 533.

Morel, B. A. (1857). Traite des degenerescences physiques, intellectuelles et morales de l”espece humaine et des causes qui produisent ces varietes maladives par le Docteur BA Morel. chez J.-B. Bailliere.

Newsome, J. (2014). Biological Theories of Crime. The Encyclopedia of Criminology and Criminal Justice, 1-5.

Plomin, R., & Spinath, F. M. (2004). Intelligence: genetics, genes, and genomics. Journal of personality and social psychology, 86(1), 112.

Portnoy, J., & Farrington, D. P. (2015). Resting heart rate and antisocial behavior: An updated systematic review and meta-analysis. Aggression and Violent Behavior, 22, 33-45. https://doi.org/10.1016/j.avb.2015.02.004

Raine, A. (2002). Annotation: The role of prefrontal deficits, low autonomic arousal, and early health factors in the development of antisocial and aggressive behavior in children. Journal of Child Psychology and Psychiatry, 43(4), 417-434. https://doi.org/10.1111/1469-7610.00034

Raine, A. (2008). From genes to brain to antisocial behavior. Current Directions in Psychological Science, 17(5), 323-328.

Sheldon, W. H., Stevens, S. S., & Tucker, W. B. (1940). The varieties of human physique.

Sheldon, W. A. (1954). Atlas of men, a guide for somatotyping the adult male at all ages.

Tielbeek, J. J., Johansson, A., Polderman, T. J. C., Rautiainen, M.-R., Jansen, P., Taylor, M., Tong, X., Lu, Q., Burt, S. A., Tiemeier, H., Viding, E., Plomin, R., Martin, N. G., Heath, A. C., Madden, P. A. F., Montgomery, G., Beaver, K. M., Waldman, I., Gelernter, J., & Posthuma, D. (2017). Genome-wide association studies of a broad spectrum of antisocial behavior. JAMA Psychiatry, 74(12), 1242-1250. https://doi.org/10.1001/jamapsychiatry.2017.3069

Viding, E., Blair, R. J. R., Moffitt, T. E., & Plomin, R. (2005). Evidence for substantial genetic risk for psychopathy in 7 year olds. Journal of Child Psychology and Psychiatry, 46(6), 592-597.

Walters, G. D., & White, T. W. (1989). Heredity and crime: Bad genes or bad research? Criminology, 27(3), 455-486. https://doi.org/10.1111/j.1745-9125.1989.tb01042.x

Wilson, M., & Daly, M. (1985). Competitiveness, risk taking, and violence: The young male syndrome. Ethology and Sociobiology, 6(1), 59-73. https://doi.org/10.1016/0162-3095(85)90041-x

Further Reading

• Cesare Lombroso: Theory of Crime, Criminal Man, and Atavism
• Zembroski, D. (2011). Sociological theories of crime and delinquency. Journal of Human Behavior in the Social Environment, 21(3), 240-254.