Biosocial Criminology

Biosocial criminology is an interdisciplinary field that examines how biological factors — genetics, neuroscience, hormones, neurochemistry, and prenatal development — interact with social and environmental factors to produce criminal and antisocial behavior. Distinguished from earlier biological theories of crime by its explicit rejection of biological determinism and its insistence on gene-environment interaction as the fundamental unit of analysis, biosocial criminology within Criminology Theories has emerged since the 1990s as one of the most rapidly growing and methodologically sophisticated areas of criminological research. Building on advances in behavioral genetics, molecular genetics, neuroscience, and epigenetics, biosocial criminologists argue that crime cannot be fully explained by either biological or social factors alone but only by their dynamic interaction — that genes shape how individuals respond to environmental conditions, and that environments shape how genes are expressed. This article traces the emergence of biosocial criminology from the older tradition of biological positivism, examines its core research domains — behavioral genetics, molecular genetics, neuroscience, and epigenetics — surveys the empirical evidence, and assesses the field’s ethical concerns, criticisms, and implications for criminal justice policy.

Outline

I. Introduction

II. From Biological Positivism to Biosocial Criminology

• a. The Legacy of Lombroso and Early Biological Theories
• b. The Rejection of Determinism
• c. The Biosocial Synthesis: Mednick, Moffitt, and Raine

III. Behavioral Genetics

• a. Twin Studies: Heritability of Antisocial Behavior
• b. Adoption Studies
• c. What Heritability Means and Does Not Mean

IV. Molecular Genetics and Gene-Environment Interaction

• a. The MAOA Gene and Childhood Maltreatment
• b. Other Candidate Genes and Polymorphisms
• c. Genome-Wide Approaches

V. Neuroscience and Neurocriminology

• a. Brain Structure and Function: Prefrontal Cortex and Amygdala
• b. Autonomic Nervous System Functioning
• c. Neurochemistry: Serotonin, Dopamine, and Cortisol

VI. Epigenetics and Early Life Adversity

• a. Epigenetic Mechanisms
• b. Childhood Adversity and Gene Expression
• c. Intergenerational Transmission of Trauma

VII. Biosocial Perspectives on Key Criminological Concepts

• a. Self-Control as a Biosocial Construct
• b. Aggression, Impulsivity, and Emotional Regulation
• c. Desistance and Biological Maturation

VIII. Ethical Concerns and Controversies

• a. Race, Biology, and the Eugenics Legacy
• b. Free Will, Responsibility, and Criminal Law
• c. Privacy, Prediction, and Genetic Surveillance

IX. Criticisms and Limitations

• a. The Replication Crisis and Candidate Gene Research
• b. Sociological Resistance
• c. The Gap Between Science and Policy

X. Policy Implications

• a. Prevention Through Early Intervention
• b. Nutrition, Prenatal Care, and Environmental Toxins
• c. Neuroscience-Informed Rehabilitation

XI. Conclusion

XII. References

Introduction

Are some individuals biologically predisposed to criminal behavior? Can genetics, brain structure, or neurochemistry explain why some people commit crimes while others in similar social circumstances do not? And if biological factors contribute to crime, what are the implications for criminal justice — for questions of responsibility, punishment, treatment, and prevention? These questions have been asked since the origins of criminology, but the answers available today are fundamentally different from those offered by the biological determinists of the nineteenth and early twentieth centuries.

Biosocial criminology within Criminology Theories represents a paradigm shift from the older biological positivism associated with Lombroso, Sheldon, and the eugenics movement. Where biological positivism sought to identify the “criminal type” — the individual whose biological characteristics determined criminal behavior — biosocial criminology insists that there is no criminal gene, no criminal brain structure, and no criminal body type. Instead, there are biological characteristics — genetic polymorphisms, neural circuits, hormonal profiles, autonomic nervous system patterns — that interact with environmental conditions to increase or decrease the probability of antisocial behavior. The same genetic variant that predisposes to aggression in an abusive environment may have no effect — or even a protective effect — in a supportive one. Biology matters, but it matters only in context.

The field has grown rapidly since the publication of foundational works by Sarnoff Mednick, Terrie Moffitt, Adrian Raine, Kevin Beaver, and Anthony Walsh, and it has been supported by transformative advances in genomic technology, neuroimaging, and epigenetic research that have made it possible to study the biological correlates of behavior with unprecedented precision. This article examines the core research domains of biosocial criminology, the evidence they have produced, and the scientific, ethical, and policy questions they raise.

From Biological Positivism to Biosocial Criminology

The Legacy of Lombroso and Early Biological Theories

The study of biological contributions to crime has a troubled history. Cesare Lombroso’s (1876) theory of the “born criminal” — the atavistic individual whose physical characteristics (asymmetrical skull, prominent jaw, unusual ear shape) revealed a biological predisposition to crime — dominated criminology in the late nineteenth century but was ultimately discredited by the absence of empirical support and by its association with racial pseudoscience and the eugenics movement. Subsequent biological theories — including William Sheldon’s (1949) somatotype theory, which linked body build to temperament and criminal behavior, and the XYY chromosome hypothesis, which proposed that males with an extra Y chromosome were predisposed to violent crime — suffered similar fates: initial enthusiasm followed by empirical disconfirmation and ethical critique.

The eugenics movement represented the darkest application of biological theories of crime. Policies of forced sterilization, institutionalization, and racial segregation were justified on the grounds that criminal behavior was hereditary and that the “unfit” should be prevented from reproducing. More than 60,000 Americans were forcibly sterilized under eugenic laws, and the Nazi regime’s program of racial hygiene — which culminated in the Holocaust — drew explicitly on American eugenic theory and practice. The association between biological explanations of crime and these atrocities created a deep and understandable suspicion of biological approaches to crime that persists in some quarters of the discipline to this day.

Biosocial criminology emerged in explicit opposition to this legacy. Contemporary biosocial criminologists do not argue that criminals are biologically determined, that criminal behavior is hereditary in a simple Mendelian sense, or that biological differences between racial groups explain differences in crime rates. Instead, they argue that biological factors — genes, brain structure, neurochemistry, prenatal environment — interact with social and environmental factors to influence behavior, and that understanding these interactions is essential for a complete account of crime.

The Rejection of Determinism

The defining feature of biosocial criminology — and the feature that distinguishes it from the biological positivism of Lombroso and his successors — is its explicit rejection of biological determinism. Biosocial criminologists insist that genes do not determine behavior; they influence the probability of behavior by shaping how individuals respond to environmental conditions. Walsh and Beaver (2009) characterized biosocial criminology as the study of how “genes set us on particular developmental trajectories, but the vagaries of the environment can send those trajectories askew.”

This interactionist framework draws on the concept of gene-environment interaction (G×E) — the principle that the effect of a genetic variant on behavior depends on the environmental context in which the individual develops. A genetic predisposition to aggression may be expressed as violent behavior in an abusive, neglectful, or impoverished environment but may remain latent — or be channeled into socially acceptable forms of assertiveness — in a supportive, well-resourced environment. The same gene, in different environments, can produce dramatically different behavioral outcomes.

The rejection of determinism has important ethical and policy implications. If biological factors contribute to crime only in interaction with environmental conditions, then the most effective crime prevention strategies are not biological interventions (genetic screening, pharmacological suppression, neurosurgery) but social and environmental interventions that alter the conditions under which biological risk factors are expressed. Improving prenatal care, reducing childhood adversity, eliminating lead exposure, providing adequate nutrition, and building supportive family and community environments are all strategies that can reduce the expression of biological risk factors without targeting or stigmatizing individuals on the basis of their biology.

The Biosocial Synthesis: Mednick, Moffitt, and Raine

Three scholars played pivotal roles in establishing biosocial criminology as a legitimate field of inquiry. Sarnoff Mednick’s pioneering research on adoption studies in Denmark during the 1980s provided some of the earliest rigorous evidence that genetic factors contribute to criminal behavior independently of the family environment in which individuals are raised. Mednick, Gabrielli, and Hutchings (1984) found that adopted children whose biological parents had criminal records were significantly more likely to have criminal records themselves than adopted children whose biological parents had no criminal records — even when the adoptive family environment was controlled. This finding provided evidence for a genetic contribution to criminal behavior that could not be attributed to shared family environment.

Terrie Moffitt’s (1993) developmental taxonomy — which distinguished between “life-course-persistent” offenders (whose antisocial behavior begins in childhood and persists across the lifespan) and “adolescence-limited” offenders (whose antisocial behavior is confined to the teenage years) — provided the theoretical framework that integrated biological and social explanations of crime within a developmental model. Moffitt argued that life-course-persistent offenders are characterized by neuropsychological deficits — subtle impairments in verbal ability, executive functioning, and self-regulation — that originate in prenatal and perinatal risk factors (maternal substance use, birth complications, nutritional deficiencies) and that interact with disadvantaged family and neighborhood environments to produce persistent antisocial behavior. Adolescence-limited offenders, by contrast, are neuropsychologically normal individuals whose delinquency reflects the social dynamics of adolescence rather than underlying biological vulnerability.

Adrian Raine’s (1993, 2013) program of neurocriminological research provided the most detailed empirical mapping of the brain structures, autonomic nervous system patterns, and neurochemical profiles associated with antisocial and violent behavior. Raine’s work, culminating in The Anatomy of Violence (2013), demonstrated that reduced prefrontal cortex functioning, low resting heart rate, and abnormal amygdala reactivity are among the most consistent biological correlates of persistent antisocial behavior — correlates that interact with environmental risk factors (childhood abuse, poverty, social deprivation) to produce criminal outcomes.

Behavioral Genetics

Twin Studies: Heritability of Antisocial Behavior

Behavioral genetics studies — particularly twin studies and adoption studies — have provided the most systematic evidence for the role of genetic factors in antisocial behavior. Twin studies compare the concordance rates for criminal or antisocial behavior between monozygotic (identical) twins, who share 100 percent of their genetic material, and dizygotic (fraternal) twins, who share approximately 50 percent. If genetic factors contribute to antisocial behavior, monozygotic twins should show higher concordance than dizygotic twins.

Meta-analyses of twin studies have consistently found that genetic factors account for approximately 40–60 percent of the variance in antisocial behavior, with shared environmental factors (family environment, socioeconomic status) accounting for a smaller proportion and nonshared environmental factors (peer influences, individual experiences, stochastic developmental processes) accounting for the remainder (Rhee & Waldman, 2002; Ferguson, 2010). These heritability estimates are comparable to those found for other complex behavioral traits, including intelligence, personality, and mental health conditions.

The heritability of antisocial behavior is not uniform across subtypes or developmental stages. Genetic influences are generally stronger for persistent, aggressive, and life-course-persistent patterns of antisocial behavior than for transient, non-aggressive, and adolescence-limited patterns (Baker, Bezdjian, & Raine, 2006). The genetic contribution to antisocial behavior also appears to increase with age — a pattern consistent with the developmental principle that genetic influences become more pronounced as individuals increasingly select and shape their own environments in ways that correspond to their genetic predispositions.

Adoption Studies

Adoption studies complement twin studies by examining individuals who are raised apart from their biological parents, allowing researchers to separate the contributions of genetic inheritance and family environment. If adopted children resemble their biological parents (with whom they share genes but not environment) more than their adoptive parents (with whom they share environment but not genes), then genetic factors are implicated in the transmission of the trait.

Mednick et al. (1984), in the largest adoption study of criminal behavior, examined the criminal records of 14,427 Danish adoptees and their biological and adoptive parents. They found that adoptees whose biological parents had criminal convictions were significantly more likely to have criminal convictions themselves — a genetic effect that was independent of the adoptive family environment. The effect was strongest for property crime and weakest for violent crime, and it was moderated by the adoptive family environment: adoptees with both genetic risk (biological parent criminal) and environmental risk (adoptive parent criminal) had the highest rates of criminal conviction.

Cadoret, Yates, Troughton, Woodworth, and Stewart (1995) found similar results in a sample of Iowa adoptees, demonstrating that both biological parent antisocial behavior and adverse adoptive family environments predicted offspring conduct problems — and that the effects were interactive rather than merely additive. These adoption studies provided strong evidence that genetic factors contribute to antisocial behavior and that their effects are moderated by the environmental conditions in which individuals develop — the core proposition of biosocial criminology.

What Heritability Means and Does Not Mean

The concept of heritability has been widely misunderstood in both popular and scholarly discussions of biosocial criminology. Heritability is a population statistic, not an individual characteristic: it describes the proportion of the variance in a trait within a specific population that is attributable to genetic differences among individuals in that population at a given time and place. It does not describe the proportion of an individual’s behavior that is caused by genes, and it does not imply that the trait is immutable, inevitable, or impervious to environmental influence.

A heritability estimate of 50 percent for antisocial behavior does not mean that half of an individual’s criminal conduct is genetically caused. It means that, within the population studied, approximately half of the individual differences in antisocial behavior can be statistically attributed to genetic differences among individuals — with the other half attributable to environmental differences. If the environmental conditions changed dramatically (if poverty were eliminated, abuse were prevented, and all children received optimal nutrition and education), the heritability estimate would change as well — because the environmental variation that currently contributes to individual differences would be reduced.

This point has critical implications for policy. High heritability does not mean that a trait is unchangeable; it means that, within the current range of environmental variation, genetic differences make a substantial contribution to individual differences. Altering the environment — particularly by reducing the adverse conditions that trigger the expression of genetic risk factors — can reduce the incidence of antisocial behavior even when its heritability is high. Biosocial criminology’s policy implications point toward environmental intervention, not genetic selection.

Molecular Genetics and Gene-Environment Interaction

The MAOA Gene and Childhood Maltreatment

The most influential finding in molecular biosocial criminology is Caspi, McClay, Moffitt, Mill, Martin, Craig, Taylor, and Poulton’s (2002) discovery of a gene-environment interaction involving the monoamine oxidase A (MAOA) gene and childhood maltreatment. Using longitudinal data from the Dunedin Multidisciplinary Health and Development Study — a cohort of approximately 1,000 New Zealand males followed from birth to adulthood — Caspi and colleagues found that a polymorphism in the MAOA gene moderated the impact of childhood maltreatment on antisocial behavior. Males with the low-activity variant of the MAOA gene who had experienced severe childhood maltreatment were significantly more likely to develop conduct disorder, be convicted of violent crime, and exhibit antisocial personality traits than males with the high-activity variant who had experienced similar maltreatment. Maltreated males with the high-activity variant showed levels of antisocial behavior no higher than the non-maltreated comparison group.

This finding was groundbreaking because it demonstrated that the relationship between a specific gene and antisocial behavior is not direct but conditional — the gene affects behavior only in the presence of a specific environmental trigger (childhood maltreatment). The MAOA finding provided a concrete, empirically documented example of the gene-environment interaction that biosocial criminology had long theorized and helped legitimize the biosocial approach within mainstream criminology.

A meta-analysis by Kim-Cohen, Caspi, Taylor, Williams, Newcombe, Craig, and Moffitt (2006) confirmed the MAOA × maltreatment interaction across multiple studies and samples, although subsequent replication attempts have produced mixed results — with some studies confirming the interaction and others failing to replicate it. The inconsistency of replication has become a significant concern in the field and has contributed to broader debates about the reliability of candidate gene research.

Other Candidate Genes and Polymorphisms

Research on candidate genes beyond MAOA has examined the role of several other genetic variants in antisocial behavior. Polymorphisms in the serotonin transporter gene (5-HTTLPR), which affects the regulation of serotonin — a neurotransmitter implicated in mood regulation, impulsivity, and aggression — have been examined in relation to depression, aggression, and antisocial behavior. Dopamine receptor genes (DRD2, DRD4) and the dopamine transporter gene (DAT1), which affect the brain’s reward system, have been studied in relation to sensation-seeking, impulsivity, and substance use.

The results of candidate gene research have been mixed and, in many cases, disappointing. Initial reports of significant associations between specific polymorphisms and antisocial behavior have frequently failed to replicate in larger, more rigorous studies. The candidate gene approach has been criticized for its reliance on small sample sizes, multiple testing without adequate correction, and the selection of genes based on plausible biological mechanisms rather than unbiased genomic evidence (Duncan & Keller, 2011). These concerns have led to a shift toward genome-wide approaches that examine the effects of many genetic variants simultaneously.

Despite these limitations, the candidate gene literature has established an important principle: the effects of individual genetic variants on complex behavioral outcomes such as crime are very small — typically accounting for less than 1 percent of the variance in behavior. Antisocial behavior, like all complex traits, is influenced by thousands of genetic variants, each with a tiny individual effect, in combination with environmental factors that shape their expression. This polygenic architecture implies that there is no single “crime gene” and that genetic contributions to criminal behavior operate through the aggregate effects of many variants distributed across the genome.

Genome-Wide Approaches

The limitations of candidate gene research have motivated a shift toward genome-wide association studies (GWAS), which examine the entire genome to identify genetic variants associated with a trait without prior hypotheses about which genes are involved. GWAS studies of antisocial behavior, aggression, and related traits have identified numerous genetic loci that reach genome-wide significance — but each individual variant explains only a tiny fraction of the variance in the trait.

Tielbeek, Johansson, Polderman, Müntz, Burt,”; Bartels, Langevin,’; Raine, and others (2017) conducted one of the largest GWAS of antisocial behavior to date, using a meta-analytic approach across multiple samples. They found evidence for polygenic influences on antisocial behavior — many genetic variants, each with a very small effect, that collectively account for a meaningful proportion of the heritability. The polygenic score approach — which aggregates the effects of thousands of genetic variants into a single index of genetic risk — has shown modest but significant predictive power for antisocial behavior and related outcomes.

GWAS research has confirmed the polygenic architecture of antisocial behavior and has identified specific biological pathways (involving neurotransmitter regulation, neural development, and synaptic functioning) that contribute to genetic risk. However, the practical utility of GWAS findings for criminal justice applications remains limited: polygenic risk scores explain only a small proportion of the variance in antisocial behavior, they cannot predict individual-level outcomes with meaningful accuracy, and they raise significant ethical concerns about genetic profiling and discrimination.

Table 1. Research Domains in Biosocial Criminology

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Domain	Methods	Key Findings	Representative Studies
Behavioral genetics	Twin studies, adoption studies	~40–60% heritability for antisocial behavior; G×E interaction	Rhee & Waldman (2002); Mednick et al. (1984)
Molecular genetics	Candidate gene studies, GWAS	MAOA × maltreatment interaction; polygenic architecture	Caspi et al. (2002); Tielbeek et al. (2017)
Neuroscience	Neuroimaging (fMRI, structural MRI)	Prefrontal cortex deficits; amygdala dysfunction; low heart rate	Raine (2013); Yang et al. (2005)
Epigenetics	DNA methylation, gene expression	Childhood adversity alters gene expression; intergenerational effects	McGowan et al. (2009); Cecil et al. (2014)

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Neuroscience and Neurocriminology

Brain Structure and Function: Prefrontal Cortex and Amygdala

Neurocriminology — the study of the neural correlates of criminal and antisocial behavior — has identified several brain regions and circuits that are consistently associated with aggression, impulsivity, and violent crime. The prefrontal cortex (PFC), which is responsible for executive functioning — planning, decision-making, impulse control, emotional regulation, and the evaluation of consequences — is the brain region most consistently linked to antisocial behavior. Reduced PFC volume, reduced PFC activation during cognitive tasks, and impaired PFC connectivity with other brain regions have been found in studies of violent offenders, psychopathic individuals, and individuals with antisocial personality disorder (Raine, 2013; Yang, Raine, Lencz, Bihrle, Lacasse, & Colletti, 2005).

The amygdala — the brain region responsible for processing emotional stimuli, particularly fear and threat — has also been implicated in antisocial behavior. Individuals with psychopathic traits show reduced amygdala reactivity to fearful faces and other emotional stimuli, suggesting that impaired emotional processing contributes to the callous-unemotional traits (lack of empathy, shallow affect, failure to learn from punishment) that characterize psychopathy. The functional disconnection between the PFC and the amygdala — the failure of the prefrontal cortex to regulate the emotional responses generated by the amygdala — may be a key neural mechanism underlying impulsive aggression.

Raine’s (2013) work synthesized decades of neurocriminological research, demonstrating that the neural correlates of antisocial behavior are not deterministic — they increase risk but do not determine outcomes. Individuals with PFC deficits who grow up in supportive environments may develop compensatory strategies that prevent the expression of antisocial behavior, while individuals with intact PFC functioning who are exposed to severe adversity may develop antisocial patterns through environmental pathways. The biosocial framework insists that neural risk factors operate in interaction with social conditions rather than independently of them.

Autonomic Nervous System Functioning

Research on the autonomic nervous system (ANS) has identified low resting heart rate as one of the most consistent and best-replicated biological correlates of antisocial behavior. The association between low resting heart rate and antisocial behavior has been documented across diverse populations, age groups, and cultural contexts (Portnoy & Farrington, 2015). Low resting heart rate in childhood predicts subsequent aggressive and antisocial behavior — a prospective association that holds after controlling for socioeconomic status, family characteristics, and other confounders.

Two theoretical explanations have been proposed for this association. The fearlessness theory proposes that low autonomic arousal reflects a reduced capacity for fear — and that individuals who experience less fear are less deterred by the threat of punishment, less anxious about the consequences of their actions, and more willing to engage in risky and antisocial behavior. The stimulation-seeking theory proposes that low arousal represents an aversive physiological state — a condition of chronic underarousal that motivates individuals to seek stimulation through exciting, novel, and sometimes dangerous or criminal activities.

The ANS findings illustrate the biosocial principle that biological risk factors operate through interaction with environmental conditions. Low resting heart rate may predispose to antisocial behavior in environments where criminal opportunities are available and informal social controls are weak — but the same physiological characteristic may predispose to prosocial risk-taking (entrepreneurship, athletics, emergency response) in environments that provide legitimate outlets for sensation-seeking.

Neurochemistry: Serotonin, Dopamine, and Cortisol

Neurochemical research has examined the role of neurotransmitters and hormones in antisocial behavior. Serotonin (5-HT) — a neurotransmitter involved in mood regulation, impulse control, and aggression — is the neurochemical most consistently associated with violent behavior. Low serotonin functioning has been found in studies of violent offenders, impulsive individuals, and laboratory animals that exhibit aggressive behavior (Moffitt, Brammer, Caspi, Fawcett, Raleigh, Yuwiler, & Silva, 1998). The relationship between serotonin and aggression is mediated by the PFC: serotonergic neurons project from the brainstem to the prefrontal cortex, and reduced serotonergic input to the PFC impairs the executive functioning — particularly impulse control — that regulates aggressive behavior.

Dopamine — the neurotransmitter associated with reward, motivation, and pleasure — has been implicated in sensation-seeking, risk-taking, and substance use, all of which are associated with criminal behavior. Cortisol — the primary stress hormone — has been studied in relation to both the stress reactivity and the fear conditioning deficits associated with antisocial behavior. Low cortisol reactivity has been found in individuals with conduct disorder and callous-unemotional traits, suggesting that reduced stress responsivity contributes to the fearlessness and reward insensitivity that characterize persistent antisocial behavior.

The neurochemical research underscores the complexity of the biological contributions to crime. No single neurotransmitter or hormone causes criminal behavior; rather, the neurochemical systems interact with one another and with the neural circuits and environmental conditions that shape their effects. Interventions that target neurochemical imbalances — including pharmacological treatments for impulsivity, aggression, and emotional dysregulation — represent one potential application of neurocriminological research, but their use in criminal justice settings raises ethical concerns about coerced treatment and the medicalization of criminal behavior.

Epigenetics and Early Life Adversity

Epigenetic Mechanisms

Epigenetics — the study of changes in gene expression that do not involve alterations to the DNA sequence itself — has emerged as one of the most transformative developments in biosocial criminology. Epigenetic mechanisms — including DNA methylation, histone modification, and non-coding RNA regulation — determine which genes are active and which are silent in a given cell, at a given time, in response to environmental conditions. These mechanisms provide a molecular pathway through which environmental experiences — particularly experiences during critical developmental periods — can alter gene expression and thereby influence behavior.

The significance of epigenetics for biosocial criminology is profound. It provides the biological mechanism through which the gene-environment interaction operates: environmental conditions (nutrition, stress, toxin exposure, caregiving quality) alter the epigenetic marks on genes, which in turn alter the expression of those genes, which in turn affects the neural circuits and neurochemical systems that regulate behavior. Epigenetics thus bridges the gap between the macro-level social conditions that criminological theories identify as the causes of crime and the molecular-level processes that translate those conditions into individual behavior.

Epigenetic changes are potentially reversible — unlike mutations in the DNA sequence, epigenetic marks can be altered by subsequent environmental experiences, pharmacological interventions, or behavioral therapies. This reversibility has important implications for policy: if adverse childhood experiences produce antisocial behavior through epigenetic alterations in gene expression, then interventions that provide compensatory positive experiences — secure attachment, enriched environments, therapeutic relationships — may be able to reverse or mitigate these epigenetic effects.

Childhood Adversity and Gene Expression

McGowan, Sasaki, D’Alessio, Dymov, Labonté, Szyf, Turecki, and Meaney (2009) conducted a landmark study examining the epigenetic effects of childhood abuse on gene expression in the human brain. Analyzing postmortem brain tissue from suicide victims with and without histories of childhood abuse, they found that childhood abuse was associated with increased methylation of the glucocorticoid receptor gene (NR3C1) in the hippocampus — a modification that reduces the expression of the receptor and impairs the brain’s ability to regulate the stress response. This finding demonstrated a specific molecular mechanism through which childhood adversity alters brain function — and provided a biological explanation for the well-documented link between childhood abuse and subsequent aggression, impulsivity, and antisocial behavior.

Cecil, Viding, Barker, Guiney, and McCrory (2014) extended this research to a community sample, finding that childhood adversity (including abuse, neglect, and household dysfunction) was associated with alterations in DNA methylation across multiple genes involved in stress regulation, immune function, and neural development. These epigenetic changes were detectable in blood samples — suggesting that the biological effects of childhood adversity are not confined to the brain but affect biological systems throughout the body.

The epigenetic research on childhood adversity converges with the criminological literature on adverse childhood experiences (ACEs) — the well-documented association between childhood trauma and subsequent criminal behavior. Biosocial criminology provides the biological mechanism that explains this association: childhood adversity alters gene expression through epigenetic modifications, which impair the neural and neurochemical systems that regulate impulse control, emotional reactivity, and stress responsivity — impairments that increase the probability of antisocial behavior in subsequent developmental stages.

Intergenerational Transmission of Trauma

Among the most provocative findings in epigenetic research is the evidence for the intergenerational transmission of epigenetic modifications — the possibility that the effects of environmental experiences in one generation can be transmitted to subsequent generations through epigenetic changes in the germline (sperm and egg cells). Animal studies have demonstrated that stress, nutritional deprivation, and toxin exposure in parental animals can produce epigenetic changes that are transmitted to offspring and that affect the offspring’s behavior and stress reactivity — even when the offspring are raised in normal conditions.

The implications for criminology are potentially far-reaching. If the effects of poverty, violence, and institutional racism are transmitted not only through social mechanisms (cultural transmission, differential socialization, structural disadvantage) but also through biological mechanisms (epigenetic modifications that alter gene expression across generations), then the intergenerational concentration of criminal behavior in disadvantaged communities may reflect a biological pathway that supplements the social pathways identified by traditional criminological theories.

However, the evidence for intergenerational epigenetic transmission in humans remains preliminary, and the extension of animal findings to human populations is methodologically challenging. The field is rapidly evolving, and the criminological implications of intergenerational epigenetics are speculative at this stage. Nevertheless, the possibility that environmental adversity produces biological effects that persist across generations underscores the urgency of addressing the structural conditions — poverty, violence, discrimination, institutional neglect — that produce adversity in the first place.

Biosocial Perspectives on Key Criminological Concepts

Self-Control as a Biosocial Construct

Gottfredson and Hirschi’s (1990) self-control theory proposed that low self-control — the tendency to pursue immediate gratification without regard for long-term consequences — is the primary cause of crime. Biosocial criminologists have examined the biological underpinnings of self-control, finding that individual differences in self-control are substantially heritable (twin studies estimate heritability at approximately 50–60 percent) and are associated with specific neural circuits (particularly the prefrontal cortex) and neurochemical systems (particularly serotonin and dopamine) that regulate impulse control and delayed gratification.

Beaver, Wright, DeLisi, and Vaughn (2008) used data from the National Longitudinal Study of Adolescent Health (Add Health) to examine whether genetic factors contribute to self-control and whether the effects of self-control on criminal behavior are mediated by genetic influences. Their analysis found significant genetic contributions to both self-control and criminal behavior, and they argued that the relationship between self-control and crime is partly a product of shared genetic influences — a finding that challenges Gottfredson and Hirschi’s purely sociological account of self-control as a product of parenting.

The biosocial perspective on self-control does not reject the importance of parenting — it integrates parenting with biological factors by proposing that effective parenting and biological maturation interact to produce self-regulatory capacity. Children with biological risk factors (low serotonergic functioning, PFC deficits, low autonomic arousal) may require more intensive, structured, and responsive parenting to develop adequate self-control than children without these risk factors. The biosocial framework suggests that self-control is a product of the dynamic interaction between biological endowment and social environment rather than a purely social construction.

Aggression, Impulsivity, and Emotional Regulation

Biosocial research has examined the biological foundations of aggression — the behavioral outcome most closely associated with violent crime. The distinction between reactive aggression (impulsive, emotionally driven, threat-responsive) and proactive aggression (planned, instrumentally motivated, goal-directed) has proven important for biosocial analysis because the two types of aggression appear to have partially different biological substrates. Reactive aggression is associated with amygdala hyperreactivity, reduced PFC regulation, and low serotonergic functioning — a pattern consistent with impaired emotional regulation. Proactive aggression is associated with reduced amygdala reactivity and callous-unemotional traits — a pattern consistent with the fearlessness and emotional detachment that characterize psychopathy.

The biosocial analysis of impulsivity — the tendency to act without thinking, to seek immediate rewards, and to fail to consider the consequences of action — has identified impulsivity as a core behavioral mechanism linking biological risk factors to criminal outcomes. Impulsivity is substantially heritable, is associated with specific genetic variants (particularly in the dopamine system), and is reflected in measurable neural and autonomic patterns (reduced PFC activation, low resting heart rate, attenuated skin conductance response).

Emotional regulation — the capacity to modulate emotional responses in accordance with situational demands — is the executive function most directly relevant to the prevention of criminal behavior. Individuals who can regulate their emotional responses effectively — suppressing anger when provocation occurs, resisting temptation when criminal opportunities present themselves, managing frustration when goals are blocked — are significantly less likely to engage in criminal behavior. The biosocial research on emotional regulation has identified the neural circuits (PFC-amygdala connectivity), neurochemical systems (serotonin, cortisol), and genetic variants that underlie individual differences in regulatory capacity — providing a biological foundation for understanding why some individuals are better equipped than others to resist criminal impulses.

Desistance and Biological Maturation

The phenomenon of desistance — the decline and cessation of criminal behavior that occurs for most offenders during the transition from adolescence to adulthood — has been explained by biosocial criminologists in terms of biological maturation. The prefrontal cortex — the brain region most directly responsible for impulse control, decision-making, and the evaluation of long-term consequences — does not reach full maturity until the mid-twenties. The delayed maturation of the PFC relative to the earlier maturation of the subcortical structures (amygdala, nucleus accumbens) that generate emotional impulses and reward-seeking creates a developmental mismatch during adolescence: the drive systems are fully active, but the regulatory systems are not yet capable of controlling them.

This neurobiological perspective on desistance complements Sampson and Laub’s (1993) social explanation (which emphasizes the formation of adult social bonds through marriage and employment) by identifying the biological maturation that underlies the developmental transition. As the PFC matures during the late teens and early twenties, individuals develop greater capacity for impulse control, emotional regulation, and long-term planning — capacities that support the formation and maintenance of the social bonds that Sampson and Laub identified as the primary mechanisms of adult desistance.

The biosocial perspective on desistance has implications for the criminal justice treatment of young offenders. If the impulsive, risk-seeking, and emotionally reactive behavior that characterizes adolescent offending is partly a product of neurodevelopmental immaturity rather than stable criminal propensity, then harsh punishment — particularly incarceration during the critical period of PFC development — may be counterproductive. The Supreme Court’s decisions in Roper v. Simmons (2005), Graham v. Florida (2010), and Miller v. Alabama (2012), which limited the most severe criminal penalties for juvenile offenders, drew explicitly on neuroscientific evidence about adolescent brain development.

Table 2. Biosocial Risk Factors and Environmental Moderators

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Biological Risk Factor	Associated Outcome	Environmental Moderator	G×E Evidence
Low-activity MAOA gene	Antisocial behavior, conduct disorder	Childhood maltreatment	Caspi et al. (2002); Kim-Cohen et al. (2006)
Low resting heart rate	Aggression, persistent antisocial behavior	Environmental adversity	Portnoy & Farrington (2015)
Reduced PFC volume/activation	Impulsivity, poor decision-making	Supportive vs. adverse caregiving	Raine (2013)
Low serotonergic functioning	Impulsive aggression	Stressful environments	Moffitt et al. (1998)
Epigenetic modifications (NR3C1)	Impaired stress regulation	Childhood abuse and neglect	McGowan et al. (2009)

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Ethical Concerns and Controversies

Race, Biology, and the Eugenics Legacy

The most sensitive ethical issue in biosocial criminology is the relationship between biology, race, and crime. The field’s association with the eugenics legacy — and the historical use of biological arguments to justify racial discrimination, forced sterilization, and genocide — creates a responsibility for biosocial criminologists to address racial implications with exceptional care. Walsh and Beaver (2009) have argued that biosocial criminology does not support racial explanations of crime — that the genetic variants associated with antisocial behavior are distributed across all racial groups and that racial differences in crime rates are best explained by differential exposure to the environmental conditions (poverty, discrimination, neighborhood disadvantage) that trigger the expression of biological risk factors.

Nevertheless, some biosocial research has been criticized for its potential to provide scientific legitimacy for racial explanations of crime. The finding that certain genetic variants (such as the low-activity MAOA allele) are more common in some racial groups than others has been misinterpreted — in both popular and scholarly discussions — as evidence that certain racial groups are genetically predisposed to violence. Biosocial criminologists have responded that allele frequencies tell us nothing about individual behavior or group-level crime rates, that the same alleles interact with environmental conditions in ways that make racial generalizations scientifically meaningless, and that the environmental conditions that activate biological risk factors (poverty, maltreatment, toxin exposure) are themselves products of structural racism and historical injustice.

The ethical obligation of biosocial criminologists extends beyond avoiding racial misinterpretation to actively confronting the structural conditions that produce both the environmental adversity and the biological risk that their research documents. A biosocial criminology that documents the biological effects of poverty, racism, and institutional neglect without advocating for the elimination of these conditions would be ethically incomplete.

Free Will, Responsibility, and Criminal Law

Biosocial criminology raises fundamental questions about free will, moral responsibility, and the foundations of criminal law. The criminal law presumes that individuals are rational agents who choose to commit crimes and who can therefore be held morally responsible for their choices. If criminal behavior is influenced by genetic predispositions, neural deficits, and neurochemical imbalances that the individual did not choose and cannot control, then the presumption of free choice on which criminal responsibility is based may be undermined.

Glenn and Raine (2014) examined the implications of neurocriminological research for criminal punishment, arguing that the growing understanding of the biological contributors to crime may eventually require a fundamental rethinking of the retributive justification for punishment. If an individual’s violent behavior is partly attributable to PFC deficits caused by prenatal alcohol exposure, childhood maltreatment, or genetic vulnerability, then punishing that individual as if they had freely chosen to act violently raises questions of justice.

However, most biosocial criminologists do not argue for the elimination of criminal responsibility. They recognize that biological influences on behavior are probabilistic, not deterministic — that even individuals with substantial biological risk factors retain the capacity for choice and that social conditions play a crucial role in determining whether biological risk is expressed as criminal behavior. The policy implication is not the abolition of criminal responsibility but the development of a criminal justice system that takes biological factors into account in sentencing, treatment, and rehabilitation — providing interventions that address the specific neurobiological vulnerabilities that contribute to individual offending patterns.

Privacy, Prediction, and Genetic Surveillance

Advances in genetic and neuroscientific technology raise concerns about the potential use of biological data for prediction, surveillance, and social control. The prospect of genetic screening to identify individuals at risk for criminal behavior, neuroimaging to assess dangerousness, or biomarker testing to predict recidivism raises profound questions about privacy, discrimination, and the appropriate limits of state power.

Biosocial criminologists have generally argued that the current state of the science does not support the use of biological data for individual-level prediction or criminal justice decision-making. Polygenic risk scores and neuroimaging markers explain only a small proportion of the variance in antisocial behavior at the population level and cannot predict individual outcomes with sufficient accuracy to justify their use in sentencing, parole, or risk assessment decisions. The risk of false positives — individuals identified as high-risk who would never have committed crimes — is too high to justify the civil liberties infringements that predictive biological screening would entail.

The ethical concerns extend to the potential for biological data to be used in ways that exacerbate existing inequalities. If genetic or neurobiological risk assessment tools are deployed within a criminal justice system already characterized by racial and class-based disparities, they may compound rather than reduce those disparities — particularly if the biological risk factors being measured are themselves products of the poverty, discrimination, and institutional neglect that disadvantaged populations disproportionately experience.

Criticisms and Limitations

The Replication Crisis and Candidate Gene Research

Biosocial criminology has been affected by the broader replication crisis in behavioral genetics and social science. Many of the candidate gene findings that generated initial excitement — including some replications of the MAOA × maltreatment interaction — have failed to replicate in larger, more rigorous studies (Duncan & Keller, 2011). The shift from candidate gene studies to genome-wide approaches has revealed that the effects of individual genetic variants on behavior are much smaller than early studies suggested, and that many published findings were likely inflated by small sample sizes, publication bias, and multiple testing.

The replication problems do not invalidate the biosocial approach — the evidence from twin studies and adoption studies for genetic contributions to antisocial behavior remains strong and well-replicated. Rather, they suggest that the specific molecular mechanisms linking genes to behavior are more complex, more polygenic, and more environmentally contingent than early candidate gene research assumed. The field is adapting to these challenges through larger samples, more rigorous statistical methods, pre-registration of hypotheses, and the use of polygenic approaches that aggregate small effects across the genome.

The replication crisis has also prompted productive self-reflection within the biosocial community about the appropriate interpretation and communication of genetic findings. Overstatement of the certainty and magnitude of gene-behavior associations — particularly in popular media — has contributed to public misunderstanding of what biosocial research has and has not established, and to the persistence of biological determinist interpretations that the field explicitly rejects.

Sociological Resistance

Biosocial criminology has encountered significant resistance from sociologically oriented criminologists who view the introduction of biological variables as a threat to the discipline’s sociological identity and as a potential vehicle for the resurgence of biological determinism. Critics have argued that biosocial criminology reductively explains complex social phenomena in biological terms, that it diverts attention and resources from the structural causes of crime (poverty, inequality, racism), and that its findings may be used to justify discriminatory policies.

Walsh and Beaver (2009) and Raine (2013) have responded that the resistance reflects a misunderstanding of the biosocial approach, which does not deny the importance of social factors but insists that biological factors also matter and that ignoring them produces an incomplete and potentially misleading account of criminal behavior. They argue that the integration of biological and social variables represents scientific progress rather than ideological regression, and that criminology cannot afford to ignore the findings of genetics, neuroscience, and epigenetics indefinitely.

The sociological resistance has diminished over time as biosocial research has become more methodologically sophisticated and as prominent sociological criminologists — including Sampson, Moffitt, and Wikström — have incorporated biological variables into their own research programs. The trajectory of the field suggests that the integration of biological and social perspectives is increasingly accepted as a necessary feature of contemporary criminological science, even if debates about the relative importance of biological and social factors continue.

The Gap Between Science and Policy

A significant limitation of biosocial criminology is the gap between its scientific findings and their practical application to criminal justice policy. While the evidence for biological contributions to antisocial behavior is substantial, the translation of this evidence into specific, actionable policy recommendations remains challenging. The effects of individual genetic variants and neurobiological markers on behavior are too small and too context-dependent to support individual-level prediction or targeted intervention — and the ethical concerns surrounding biological profiling and surveillance limit the applicability of even the most strong findings.

The most promising policy applications of biosocial research are indirect rather than direct: they point toward environmental interventions (improving prenatal care, reducing childhood adversity, eliminating lead exposure, providing adequate nutrition) that reduce the expression of biological risk factors by altering the conditions under which those factors operate. These interventions do not require biological screening or genetic profiling — they benefit all children, regardless of their biological risk profile — and they are consistent with both the biosocial emphasis on gene-environment interaction and the broader criminological commitment to addressing the social causes of crime.

The development of more direct applications — including pharmacological treatments for impulsivity and aggression, neurofeedback interventions for PFC functioning, and biosocially informed risk assessment tools — remains an active area of research, but the ethical, legal, and practical challenges of implementing these applications in criminal justice settings have not been fully resolved.

Policy Implications

Prevention Through Early Intervention

The most important policy implication of biosocial criminology is the case for early intervention. The research on gene-environment interaction, epigenetics, and neurodevelopment converges on the conclusion that the earliest years of life — from the prenatal period through early childhood — are the critical window during which biological risk factors are either activated or buffered by environmental conditions. Interventions that improve the quality of the prenatal and early childhood environment can reduce the expression of biological risk factors and prevent the developmental cascades that lead to persistent antisocial behavior.

The Nurse-Family Partnership, the Perry Preschool Project, and other early intervention programs have been shown to reduce criminal behavior among participants — effects that biosocial criminology attributes to the programs’ success in buffering biological risk factors through improved prenatal care, enhanced parental bonding, cognitive stimulation, and reduced exposure to adversity and toxins.

The biosocial case for early intervention complements the case made by developmental criminology and life-course theory — adding a biological mechanism (the buffering of genetic and neural risk factors through environmental enrichment) to the social mechanisms (the strengthening of social bonds and the development of self-control through effective parenting) that these theories identify.

Nutrition, Prenatal Care, and Environmental Toxins

Biosocial research has identified several modifiable environmental factors that affect brain development and increase the risk of antisocial behavior. Lead exposure — which damages the developing brain and impairs impulse control, attention, and executive functioning — has been consistently linked to aggressive and antisocial behavior. The dramatic decline in childhood lead exposure following the removal of lead from gasoline and paint has been proposed as a contributing factor to the crime decline of the 1990s and 2000s (Nevin, 2007).

Prenatal exposure to alcohol, tobacco, and other substances impairs fetal brain development and increases the risk of subsequent behavioral problems, including impulsivity, aggression, and conduct disorder. Adequate maternal nutrition — particularly the intake of omega-3 fatty acids, iron, and other micronutrients essential for brain development — has been associated with better neurodevelopmental outcomes and lower rates of antisocial behavior.

These findings support policies that reduce prenatal and childhood exposure to environmental toxins, provide adequate nutrition to pregnant women and young children, and ensure access to quality prenatal care — policies that address the biological pathways to crime by improving the environmental conditions under which brain development occurs.

Neuroscience-Informed Rehabilitation

Biosocial research has implications for the design of rehabilitation programs for offenders. Cognitive-behavioral therapy (CBT) — the most effective evidence-based treatment for reducing recidivism — targets the executive functioning deficits (poor impulse control, deficient problem-solving, distorted thinking patterns) that biosocial research has linked to PFC dysfunction. The effectiveness of CBT may be partly attributable to its capacity to strengthen the neural circuits underlying self-regulation — a process that neuroscientific research terms “neuroplasticity.”

Mindfulness-based interventions, which have shown promise in reducing aggression and impulsivity among incarcerated populations, may operate through similar neuroscientific mechanisms — strengthening PFC activation and PFC-amygdala connectivity through repeated practice of attentional control and emotional regulation. Pharmacological interventions that target neurochemical imbalances (particularly serotonergic and dopaminergic dysfunction) may complement behavioral therapies for individuals with severe impulsivity or aggression.

The biosocial perspective on rehabilitation suggests that treatment programs should be tailored to the specific neurobiological vulnerabilities of individual offenders — an approach that is consistent with the risk-need-responsivity (RNR) model’s emphasis on matching treatment intensity and modality to individual risk factors and criminogenic needs.

Conclusion

Biosocial criminology represents one of the most significant intellectual developments in contemporary criminological thought. By integrating the findings of behavioral genetics, molecular genetics, neuroscience, and epigenetics with the sociological analysis of crime, the field has established that criminal behavior is the product of the dynamic interaction between biological and social factors — that genes, brains, and hormones influence behavior, but only in context, and that the most effective crime prevention strategies are those that alter the environmental conditions under which biological risk factors are expressed.

The field has traveled a long distance from the biological determinism of Lombroso and the eugenics movement. Contemporary biosocial criminologists do not seek to identify the “criminal type” or to justify discriminatory policies on biological grounds. They seek to understand the full range of factors — biological, psychological, social, and environmental — that contribute to criminal behavior and to use this understanding to develop more effective, more humane, and more scientifically informed approaches to crime prevention, criminal justice, and rehabilitation.

The future of biosocial criminology lies in the continued development of gene-environment interaction research, the refinement of epigenetic models of intergenerational transmission, the application of neuroimaging advances to the study of desistance and treatment response, and the translation of scientific findings into evidence-based policies that address both the social and biological determinants of crime. As the technology for studying biological contributions to behavior becomes increasingly sophisticated and accessible, the integration of biological and social perspectives will become not merely an option for criminological research but a necessity.

References

1. Baker, L. A., Bezdjian, S., & Raine, A. (2006). Behavioral genetics: The science of antisocial behavior. Law and Contemporary Problems, 69(1–2), 7–46.
2. Barnes, J. C., Boutwell, B. B., & Beaver, K. M. (2015). Contemporary biosocial criminology. In A. R. Piquero (Ed.), The handbook of criminological theory (pp. 75–99). Wiley Blackwell.
3. Beaver, K. M. (2009). Biosocial criminology: A primer. Kendall Hunt.
4. Beaver, K. M., Wright, J. P., DeLisi, M., & Vaughn, M. G. (2008). Genetic influences on the stability of low self-control: Results from a longitudinal sample of twins. Journal of Criminal Justice, 36(6), 478–485. https://doi.org/10.1016/j.jcrimjus.2008.09.007
5. Cadoret, R. J., Yates, W. R., Troughton, E., Woodworth, G., & Stewart, M. A. (1995). Genetic-environmental interaction in the genesis of aggressivity and conduct disorders. Archives of General Psychiatry, 52(11), 916–924. https://doi.org/10.1001/archpsyc.1995.03950230030006
6. Caspi, A., McClay, J., Moffitt, T. E., Mill, J., Martin, J., Craig, I. W., Taylor, A., & Poulton, R. (2002). Role of genotype in the cycle of violence in maltreated children. Science, 297(5582), 851–854. https://doi.org/10.1126/science.1072290
7. Cecil, C. A. M., Viding, E., Barker, E. D., Guiney, J., & McCrory, E. J. (2014). Double disadvantage: The influence of childhood maltreatment and community violence exposure on adolescent mental health. Journal of Child Psychology and Psychiatry, 55(7), 839–848. https://doi.org/10.1111/jcpp.12213
8. DeLisi, M., & Vaughn, M. G. (2015). Ingredients for criminality require genes, temperament, and psychopathic personality. Journal of Criminal Justice, 43(4), 290–294. https://doi.org/10.1016/j.jcrimjus.2015.05.003
9. Duncan, L. E., & Keller, M. C. (2011). A critical review of the first 10 years of candidate gene-by-environment interaction research in psychiatry. American Journal of Psychiatry, 168(10), 1041–1049. https://doi.org/10.1176/appi.ajp.2011.11020191
10. Ferguson, C. J. (2010). Genetic contributions to antisocial personality and behavior: A meta-analytic review from an evolutionary perspective. Journal of Social Psychology, 150(2), 160–180. https://doi.org/10.1080/00224540903366503
11. Glenn, A. L., & Raine, A. (2014). Neurocriminology: Implications for the punishment, prediction and prevention of criminal behaviour. Nature Reviews Neuroscience, 15(1), 54–63. https://doi.org/10.1038/nrn3640
12. Gottfredson, M. R., & Hirschi, T. (1990). A general theory of crime. Stanford University Press.
13. 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. https://doi.org/10.1038/sj.mp.4001851
14. Lombroso, C. (1876/2006). Criminal man (M. Gibson & N. H. Rafter, Trans.). Duke University Press. (Original work published 1876)
15. McGowan, P. O., Sasaki, A., D’Alessio, A. C., Dymov, S., Labonté, B., Szyf, M., Turecki, G., & Meaney, M. J. (2009). Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse. Nature Neuroscience, 12(3), 342–348. https://doi.org/10.1038/nn.2270
16. Mednick, S. A., Gabrielli, W. F., & Hutchings, B. (1984). Genetic influences in criminal convictions: Evidence from an adoption cohort. Science, 224(4651), 891–894. https://doi.org/10.1126/science.6719119
17. Mednick, S. A., Moffitt, T. E., & Stack, S. A. (Eds.). (1987). The causes of crime: New biological approaches. Cambridge University Press.
18. 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
19. Moffitt, T. E., Brammer, G. L., Caspi, A., Fawcett, J. P., Raleigh, M., Yuwiler, A., & Silva, P. (1998). Whole blood serotonin relates to violence in an epidemiological study. Biological Psychiatry, 43(6), 446–457. https://doi.org/10.1016/S0006-3223(97)00340-5
20. Nedelec, J. L., Schwartz, J. A., Connolly, E. J., & Beaver, K. M. (2017). Biosocial criminology. In B. Teasdale & M. S. Bradley (Eds.), Preventing crime and violence (pp. 17–30). Springer. https://doi.org/10.1007/978-3-319-44124-5_2
21. Nevin, R. (2007). Understanding international crime trends: The legacy of preschool lead exposure. Environmental Research, 104(3), 315–336. https://doi.org/10.1016/j.envres.2007.02.008
22. 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
23. Raine, A. (1993). The psychopathology of crime: Criminal behavior as a clinical disorder. Academic Press.
24. Raine, A. (2002). Biosocial studies of antisocial and violent behavior in children and adults: A review. Journal of Abnormal Child Psychology, 30(4), 311–326. https://doi.org/10.1023/A:1015754122318
25. Raine, A. (2013). The anatomy of violence: The biological roots of crime. Pantheon.
26. Raine, A., Lencz, T., Bihrle, S., LaCasse, L., & Colletti, P. (2000). Reduced prefrontal gray matter volume and reduced autonomic activity in antisocial personality disorder. Archives of General Psychiatry, 57(2), 119–127. https://doi.org/10.1001/archpsyc.57.2.119
27. Raine, A., Venables, P. H., & Mednick, S. A. (1997). Low resting heart rate at age 3 years predisposes to aggression at age 11 years: Evidence from the Mauritius Child Health Project. Journal of the American Academy of Child and Adolescent Psychiatry, 36(10), 1457–1464. https://doi.org/10.1097/00004583-199710000-00029
28. Raine, A., Venables, P. H., & Williams, M. (1996). Better autonomic conditioning and faster electrodermal half-recovery time at age 15 years as possible protective factors against crime at age 29 years. Developmental Psychology, 32(4), 624–630. https://doi.org/10.1037/0012-1649.32.4.624
29. Rhee, S. H., & Waldman, I. D. (2002). Genetic and environmental influences on antisocial behavior: A meta-analysis of twin and adoption studies. Psychological Bulletin, 128(3), 490–529. https://doi.org/10.1037/0033-2909.128.3.490
30. Sampson, R. J., & Laub, J. H. (1993). Crime in the making: Pathways and turning points through life. Harvard University Press.
31. Sheldon, W. H. (1949). Varieties of delinquent youth: An introduction to constitutional psychiatry. Harper.
32. Tielbeek, J. J., Johansson, A., Polderman, T. J. C., Müntz, S., Burt, S. A., Bartels, M., … & Raine, A. (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
33. Walsh, A., & Beaver, K. M. (Eds.). (2009). Biosocial criminology: New directions in theory and research. Routledge.
34. Wright, J. P., Schnupp, R., Beaver, K. M., DeLisi, M., & Vaughn, M. (2012). Genes, maternal negativity, and self-control: Evidence of a gene × environment interaction. Youth Violence and Juvenile Justice, 10(3), 245–260. https://doi.org/10.1177/1541204011429573
35. Yang, Y., Raine, A., Lencz, T., Bihrle, S., Lacasse, L., & Colletti, P. (2005). Volume reduction in prefrontal gray matter in unsuccessful criminal psychopaths. Biological Psychiatry, 57(10), 1103–1108. https://doi.org/10.1016/j.biopsych.2005.01.021