The most important aspect of whether criminal behavior is maintained is the:

A growing body of literature has indicated the importance of considering neurobiological factors in the etiology of antisocial and criminal behavior. Behaviors, including criminality, are the result of complex, reciprocally influential interactions between an individual’s biology, psychology, and the social environment (Focquaert, 2018). As research progresses, the misconception that biology can predetermine criminality is being rectified. Elucidating the biological underpinnings of criminal behavior and broader, related outcomes such as antisocial behavior can provide insights into relevant etiological mechanisms. This selective review discusses three biological factors that have been examined in relation to antisocial and criminal behavior: psychophysiology, brain, and genetics.

Psychophysiology, or the levels of arousal within individuals, has become an important biological explanation for antisocial and criminal behavior. Two common psychophysiological measures are heart rate and skin conductance (i.e. sweat rate). Both capture autonomic nervous system functioning; skin conductance reflects sympathetic nervous system functioning while heart rate reflects both sympathetic and parasympathetic nervous system activity. Blunted autonomic functioning has been associated with increased antisocial behavior, including violence (Baker et al., 2009; Choy, Farrington, & Raine, 2015; Gao, Raine, Venables, Dawson, & Mednick, 2010; Portnoy & Farrington, 2015). Longitudinal studies have found low resting heart rate in adolescence to be associated with increased risk for criminality in adulthood (Latvala, Kuja-Halkola, Almqvist, Larsson, & Lichtenstein, 2015; Raine, Venables, & Williams, 1990). However, there is likely a positive feedback loop whereby blunted autonomic functioning may lead to increased antisocial/criminal behavior, which in turn may reinforce disrupted physiological activity. For example, males and females who exhibited high rates of proactive aggression (an instrumental, predatory form of aggression elicited to obtain a goal or reward) in early adolescence were found to have poorer skin conductance fear conditioning in late adolescence (Gao, Tuvblad, Schell, Baker, & Raine, 2015; Vitiello & Stoff, 1997).

Theories have been proposed to explain how blunted autonomic functioning could increase antisociality. The fearlessness hypothesis suggests that antisocial individuals, due to their blunted autonomic functioning, are not deterred from criminal behavior because they do not experience appropriate physiological responses to risky or stressful situations nor potential aversive consequences (Portnoy et al., 2014; Raine, 2002). Alternatively, the sensation-seeking hypothesis suggests that blunted psychophysiology is an uncomfortable state of being, and in order to achieve homeostasis, individuals engage in antisocial behavior to raise their arousal levels (Portnoy et al., 2014; Raine, 2002).

Another mechanism that could connect disrupted autonomic functioning to antisocial behavior is the failure to cognitively associate physiology responses with emotional states. Appropriately linking autonomic conditions to emotional states is important in socialization processes such as fear conditioning, which is thought to contribute to the development of a conscience. The somatic marker hypothesis (Bechara & Damasio, 2005) suggests that ‘somatic markers’ (e.g. sweaty palms) may reflect emotional states (e.g. anxiety) that can inform decision-making processes. Impairments in autonomic functioning could lead to risky or inappropriate behavior if individuals are unable to experience or label somatic changes and connect them to relevant emotional experiences. Indeed, psychopathic individuals exhibit somatic aphasia (i.e. the inaccurate identification and recognition of one’s bodily state; Gao, Raine, & Schug, 2012). Moreover, blunted autonomic functioning impairs emotional intelligence, subsequently increasing psychopathic traits (Ling, Raine, Gao, & Schug, 2018a). Impaired autonomic functioning and reduced emotional intelligence may impede the treatment of psychopathy (Polaschek & Skeem, 2018) and disrupt development of moral emotions such as shame, guilt, and empathy (Eisenberg, 2000). Such moral dysfunction, a strong characteristic of psychopaths, may contribute to their disproportionate impact on the criminal justice system (Kiehl & Hoffman, 2011).

While there is evidence that antisocial/criminal individuals typically exhibit abnormal psychophysiological functioning, it is important to acknowledge that there are different antisocial/criminal subtypes, and they may not share the same deficits. Whereas individuals who are high on proactive aggression may be more likely to exhibit blunted autonomic functioning, individuals who are high on reactive aggression (an affective form of aggression that is elicited as a response to perceived provocation) may be more likely to exhibit hyperactive autonomic functioning (Hubbard, McAuliffe, Morrow, & Romano, 2010; Vitiello & Stoff, 1997). This may have implications for different types of offenders, with elevated autonomic functioning presenting in reactively aggressive individuals who engage in impulsive crimes and blunted autonomic functioning presenting in proactively aggressive offenders engaging in more premediated crimes. Similarly, psychopaths who are ‘unsuccessful’ (i.e. convicted criminal psychopaths) exhibit reduced heart rate during stress while those who are ‘successful’ (i.e. non-convicted criminal psychopaths) exhibit autonomic functioning similar to non-psychopathic controls (Ishikawa, Raine, Lencz, Bihrle, & LaCasse, 2001). Despite differences among subgroups, dysfunctional autonomic functioning generally remains a reasonably well-replicated and robust correlate of antisocial and criminal behavior.

There has been increasing interest in the role of the brain in antisocial/criminal behavior. In general, research suggests that antisocial/criminal individuals tend to exhibit reduced brain volumes as well as impaired functioning and connectivity in key areas related to executive functions (Alvarez & Emory, 2006; Meijers, Harte, Meynen, & Cuijpers, 2017; Morgan & Lilienfeld, 2000), emotion regulation (Banks, Eddy, Angstadt, Nathan, & Phan, 2007; Eisenberg, 2000), decision-making (Coutlee & Huettel, 2012; Yechiam et al., 2008), and morality (Raine & Yang, 2006) while also exhibiting increased volumes and functional abnormalities in reward regions of the brain (Glenn & Yang, 2012; Korponay et al., 2017). These prefrontal and subcortical regions that have been implicated in antisocial/criminal behavior are the selective focus of this review.

Conventional criminal behavior has typically been associated with prefrontal cortex (PFC) structural aberrations and functional impairments (Brower & Price, 2001; Yang & Raine, 2009). The PFC is considered the seat of higher-level cognitive processes such as decision-making, attention, emotion regulation, impulse control, and moral reasoning (Sapolsky, 2004). In healthy adults, larger prefrontal structures have been associated with better executive functioning (Yuan & Raz, 2014). However, structural deficits and functional impairments of the PFC have been observed in antisocial and criminal individuals, suggesting that PFC aberrations may underlie some of the observed behaviors.

While many studies on brain differences related to criminal behavior have consisted of correlational analyses, lesion studies have provided some insight into causal neural mechanisms of antisocial/criminal behavior. The most well-known example of the effects of prefrontal lobe lesions is the case of Phineas Gage, who was reported to have a dramatic personality change after an iron rod was shot through his skull and damaged his left and right prefrontal cortices (Damasio, Grabowski, Frank, Galaburda, & Damasio, 1994; Harlow, 1848, 1868). Empirical studies suggest that prefrontal lesions acquired earlier in life disrupt moral and social development (Anderson, Bechara, Damasio, Tranel, & Damasio, 1999; Taber-Thomas et al., 2014). A study of 17 patients who developed criminal behavior following a brain lesion documented that while these lesions were in different locations, they were all connected functionally to regions activated by moral decisionmaking (Darby, Horn, Cushman, & Fox, 2018), suggesting that disruption of a neuromoral network is associated with criminality. Nevertheless, while lesion studies have implicated specific brain regions in various psychological processes such as moral development, generalizability is limited because of the heterogeneity of lesion characteristics, as well as subjects’ characteristics that may moderate the behavioral effects of the lesion.

In recent years, non-invasive neural interventions such as transcranial magnetic stimulation and transcranial electric stimulation have been used to manipulate activity within the brain to provide more direct causal evidence of the functions of specific brain regions with regard to behavior. These techniques involve subthreshold modulation of neuronal resting membrane potential (Nitsche & Paulus, 2000; Woods et al., 2016). Using transcranial electric stimulation, upregulation of the PFC has been found to decrease criminal intentions and increase perceptions of moral wrongfulness of aggressive acts (Choy, Raine, & Hamilton, 2018), providing support for the causal influence of the PFC on criminal behavior.

Importantly, there is evidence of heterogeneity within criminal subgroups. Successful psychopaths and white-collar offenders do not seem to display these prefrontal deficits (Raine et al., 2012; Yang et al., 2005). While unsuccessful psychopaths exhibit reduced PFC gray matter volume compared to successful psychopaths and non-offender controls, there are no prefrontal gray matter volume differences between successful psychopaths and non-offender controls (Yang et al., 2005). Similarly, while prefrontal volume deficits have been found in conventional criminals (i.e. blue-collar offenders), white-collar offenders do not exhibit frontal lobe reductions (Brower & Price, 2001; Ling et al., 2018b; Raine et al., 2012) and in fact may exhibit increased executive functioning compared to blue-collar controls (Raine et al., 2012). Lastly, antisocial offenders with psychopathy exhibited reduced gray matter volumes in the prefrontal and temporal poles compared to antisocial offenders without psychopathy and non-offenders (Gregory et al., 2012). It is therefore important to acknowledge that there are various types of antisocial and criminal behavior that may have different neurobiological etiologies.

The amygdala is an important brain region that has been implicated in emotional processes such as recognition of facial and auditory expressions of emotion, especially for negative emotions such as fear (Fine & Blair, 2000; Murphy, Nimmo-Smith, & Lawrence, 2003; Sergerie, Chochol, & Armony, 2008). Normative amygdala functioning has been thought to be key in the development of fear conditioning (Knight, Smith, Cheng, Stein, & Helmstetter, 2004; LaBar, Gatenby, Gore, LeDoux, & Phelps, 1998; Maren, 2001), and appropriate integration of the amygdala and PFC has been argued to underlie the development of morality (Blair, 2007). The amygdala is thought to be involved in stimulus-reinforcement learning that associates actions that harm others with the aversive reinforcement of the victims’ distress and in recognizing threat cues that typically deter individuals from risky behavior. However, amygdala maldevelopment can lead to a diminished ability to recognize distress or threat cues; disrupting the stimulus-reinforcement learning that discourages antisocial/criminal behavior (Blair, 2007; Sterzer, 2010). Indeed, while reduced amygdala volume in adulthood has been associated with increased aggressive and psychopathic characteristics from childhood to early adulthood, it is also associated with increased risk for future antisocial and psychopathic behavior (Pardini, Raine, Erickson, & Loeber, 2014).

Although the amygdala has been implicated in criminal behavior, there may be important differences between subtypes of offenders. Whereas psychopathic antisocial individuals may be more likely to exhibit cold, calculating forms of aggression, non-psychopathic antisocial individuals may be more likely to engage in impulsive, emotionally-reactive aggression (Glenn & Raine, 2014). Research suggests the former may exhibit amygdala hypoactivity and the latter, amygdala hyperactivity (Raine, 2018a). Indeed, violent offenders have been found to exhibit increased amygdala reactivity in response to provocations (da Cunha-Bang et al., 2017). Spousal abusers have also been found to exhibit increased amygdala activation when responding to aggressive words compared to nonabusers (Lee, Chan, & Raine, 2008). In a community sample of healthy adults, psychopathy scores were negatively related to amygdala reactivity while antisocial personality disorder scores were positively associated with amygdala reactivity after adjusting for overlapping variance between psychopathy and antisocial personality disorder (Hyde, Byrd, Votruba-Brzal, Hariri, & Manuck, 2014). Nevertheless, more research is needed to determine whether the presence of callous-unemotional traits (e.g. lack of guilt; Lozier, Cardinale, VanMeter, & Marsh, 2014; Viding et al., 2012) or severity of antisocial behavioral traits (Dotterer, Hyde, Swartz, Hariri, & Williamson, 2017; Hyde et al., 2016) are most relevant to the observed amygdala hypo-reactivity.

The striatum has recently garnered more attention as a region that could be implicated in the etiology of criminal behavior because of its involvement in reward and emotional processing (Davidson & Irwin, 1999; Glenn & Yang, 2012). Dysfunction in the striatum has been hypothesized to be a neural mechanism that underlies the impulsive/antisocial behavior of criminals. Indeed, individuals with higher impulsive/antisocial personality traits have been found to exhibit increased activity in the striatum (Bjork, Chen, & Hommer, 2012; Buckholtz et al., 2010; Geurts et al., 2016). Psychopathic individuals, compared to non-psychopathic individuals, demonstrate a 9.6% increase in striatal volumes (Glenn, Raine, Yaralian, & Yang, 2010). Moreover, striatal enlargement and abnormal functional connectivity of the striatum has specifically been associated with the impulsive/antisocial dimension of psychopathy (Korponay et al., 2017), suggesting this dimension of psychopathy is related to reward processes (Hare, 2017).

While much of the literature on striatal abnormalities in antisocial individuals has focused on psychopathic individuals, there is some evidence that offenders in general exhibit striatal abnormalities. Increased volume (Schiffer et al., 2011) and increased reactivity to provocations (da Cunha-Bang et al., 2017) have both been found in violent offenders as compared to non-offendersMoreover, weak cortico-striatal connectivity has been associated with increased frequency of criminal convictions (Hosking et al., 2017). In contrast, one study found reduced striatal activity to be associated with antisocial behavior (Murray, Shaw, Forbes, & Hyde, 2017). While more research is needed, current literature suggests that striatal deviations are linked to criminal behavior. One important consideration for future studies is to determine a consistent operationalization for the striatum, as some studies examine the dorsal striatum (i.e. putamen and caudate; Yang et al., 2015), others assess the corpus striatum (i.e. putamen, caudate, and globus pallidus; Glenn et al., 2010), and still others analyze the role of the ventral striatum (i.e. nucleus accumbens and olfactory tubercle; Glenn & Yang, 2012) in relation to antisocial/criminal behavior.

Abnormalities in brain regions other than the PFC, amygdala, and striatum are also associated with antisocial behavior. The neuromoral theory of antisocial behavior, first proposed by Raine and Yang (2006), argued that the diverse brain regions impaired in offenders overlap significantly with brain regions involved in moral decision-making. A recent update of this theory (Raine, 2018b) argues that key areas implicated in both moral decision-making and the spectrum of antisocial behaviors include frontopolar, medial, and ventral PFC regions, and the anterior cingulate, amygdala, insula, superior temporal gyrus, and angular gyrus/temporoparietal junction. It was further hypothesized that different manifestations of antisocial behavior exist on a spectrum of neuromoral dysfunction, with primary psychopathy, proactive aggression, and life-course persistent offending being more affected, and secondary psychopathy, reactive aggression, and crimes involving drugs relatively less affected. Whether the striatum is part of the neural circuit involved in moral decision-making is currently unclear, making its inclusion in the neuromoral model debatable. Despite limitations, the neuromoral model provides a way of understanding how impairments to different brain regions can converge on one concept – impaired morality – that is a common core to many different forms of antisocial behaviors.

One implication of the model is that significant impairment to the neuromoral circuit could constitute diminished criminal responsibility. Given the importance of a fully developed emotional moral capacity for lawful behavior, moral responsibility would appear to require intactness of neuromoral circuity. To argue that the brain basis to moral thinking and feeling are compromised in an offender comes dangerously close to challenging moral responsibility, a concept which in itself may be just a short step removed from criminal responsibility.

There is increasing evidence fora genetic basis of antisocial/criminal behavior. Behavioral genetic studies of twins and adoptees have been advantageous because such designs can differentiate the effects of genetics and environment within the context of explaining variance within a population (Glenn & Raine, 2014). Additionally, a variety of psychological and psychiatric constructs associated with antisociality/criminality, such as intelligence, personality, and mental health disorders, have been found to be heritable (Baker, Bezdjian, & Raine, 2006). While individual study estimates vary, meta-analyses have suggested the level of heritability of antisocial behavior is approximately 40–60% (Raine, 2013). Shared environmental factors have been estimated to explain approximately 11–14% of the variance in antisocial/criminal behavior and non-shared environmental influences approximately 31–37% (Ferguson, 2010; Gard, Dotterer, & Hyde, 2019). However, the heritability of antisocial/criminal behaviors vary in part based upon the specific behaviors examined (Burt, 2009; Gard et al., 2019).

Inspired by prominent theories of the neurobiology of aggression, there have been several candidate genes implicated in the serotonergic and catecholaminergic neurobiological systems that have been examined in relation to antisocial/criminal behavior (Tiihonen et al., 2015). However, a meta-analysis of genetic variants related to antisocial/criminal behavior yielded null results at the 5% significance level (Vassos, Collier, & Fazel, 2014). Nevertheless, genes do not operate in isolation, thus it is important to consider the context in which genes are activated.

Gene-environment (G x E) interactions have garnered increasing attention over the years, as these can increase risk for antisocial behavior and/or produce epigenetic changes within individuals. Longitudinal studies and meta-analyses have documented the moderating effect of the monoamine oxidase A (MAOA) gene on the relationship between maltreatment and antisocial behaviors, with the maltreatment-antisocial behavior relationship being stronger for individuals with low MAOA than high MAOA (Byrd & Manuck, 2014; Caspi et al., 2002; Fergusson, Boden, & Horwood, 2011; Kim-Cohen et al.,2006). Similarly, in a large study of African-American females, having the A1 allele of the DRD2 gene or a criminal father did not individually predict antisocial outcomes, but having both factors increased risk for serious delinquency, violent delinquency, and police contacts (Delisi, Beaver, Vaughn, & Wright, 2009). This type of G x E interaction reflects how genotypes can influence individuals’ sensitivity to environmental stressors. However, there may be important subgroup differences to consider when examining genetic risk for criminal behavior. For example, low-MAOA has been associated with higher risk for violent crime in incarcerated Caucasian offenders but not incarcerated non-Caucasian offenders (Stetler et al., 2014). Additionally, high-MAOA may protect abused and neglected Caucasians from increased risk of becoming violent or antisocial, but this buffering effect was not found for abused and neglected non-Caucasians (Widom & Brzustowicz, 2006). Thus, while the MAOA gene has been associated with antisocial/criminal behavior, there are still nuances of this relationship that should be considered (Goldman & Rosser, 2014).

Another way in which G x E interactions manifest themselves is when environmental stressors result in epigenetic changes, thus becoming embedded in biology that result in long-term symptomatic consequences. For example, females exposed to childhood sex abuse have exhibited alterations in the methylation of the 5HTT promoter region, which in turn has been linked to subsequent antisocial personality disorder symptoms (Beach, Brody, Todorov, Gunter, & Philibert, 2011). There has been a growing body of work on such epigenetic mechanisms involved in the biological embedding of early life stressors and transgenerational trauma (Kellermann, 2013; Provencal & Binder, 2015). Thus, just as biological mechanisms can influence environmental responses, environmental stressors can affect biological expressions.

While genes may interact with the environment to produce antisocial/criminal outcomes, they can also interact with other genes. There is evidence that dopamine genes DRD2 and DRD4 may interact to increase criminogenic risk (Beaver et al., 2007; Boutwell et al., 2014). The effect of the 7-repeat allele DRD4 is strengthened in the presence of the A1 allele of DRD2, and has been associated with increased odds of committing major theft, burglary, gang fighting, and conduct disorder (Beaver et al., 2007; Boutwell et al., 2014). However, there is some evidence that DRD2 and DRD4 do not significantly affect delinquency abstention for females (Boutwell & Beaver, 2008). Thus there may be demographic differences that moderate the effect of genetic interactions on various antisocial outcomes (Dick, Adkins, & Kuo, 2016; Ficks & Waldman, 2014; Rhee & Waldman, 2002; Salvatore & Dick, 2018), and such differences warrant further research.

Importantly, biological correlates of antisocial and criminal behavior are inextricably linked in dynamical systems, in which certain processes influence others through feedback loops. While a detailed summary is beyond the scope of this review, some interactions between biological mechanisms are briefly illustrated here. Within the brain, the PFC and amygdala have reciprocal connections, with the PFC often conceptualized as monitoring and regulating amygdala activity (Gillespie, Brzozowski, & Mitchell, 2018). Disruption of PFC-amygdala connectivity has been linked to increased antisocial/criminal behavior, typically thought to be due to the impaired top-down regulation of amygdala functioning by the PFC. Similarly, the brain and autonomic functioning are linked (Critchley, 2005; Wager et al., 2009); output from the brain can generate changes in autonomic functioning by affecting the hypothalamic-pituitary-adrenal axis, but autonomic functions also provide input to the brain that is essential for influencing behavioral judgments and maintaining coordinated regulation of bodily functions (Critchley, 2005). While not comprehensive, these examples illustrate that biological systems work together to produce behavior.

While biological processes can contribute to antisocial/criminal behavior, these do not guarantee negative outcomes. Considering that many of the aforementioned biological risk factors are significantly influenced by social environment, interventions in multiple spheres may help mitigate biological risks for antisocial behavior.

With regard to psychophysiological correlates of antisocial behavior, research suggests differential profiles of arousal impairment depending on the type of antisocial behavior (Hubbard et al., 2010; Vitiello & Stoff, 1997). Treatments designed to address the issues associated with psychophysiological differences are typically behavioral in nature, targeted at associated symptoms. Studies of mindfulness have suggested its utility in improving autonomic functioning (Delgado-Pastor, Perakakis, Subramanya, Telles, & Vila, 2013) and emotion regulation (Umbach, Raine, & Leonard, 2018), which may better help individuals with reactive aggression and hyperarousal. Hypo-arousal has been associated with impaired emotional intelligence (Ling et al., 2018a), but emotional intelligence training programs have shown some promise in reducing aggression and increasing empathy among adolescents and increasing emotional intelligence among adults (Castillo, Salguero, Fernandez-Berrocal, & Balluerka, 2013; Hodzic, Scharfen, Ropoll, Holling, & Zenasni, 2018), and in reducing recidivism (Megreya, 2015; Sharma, Prakash, Sengar, Chaudhury, & Singh, 2015).

Regarding healthy neurodevelopment, research has supported a number of areas to target. Poor nutrition, both in utero and in early childhood, have been associated with negative and criminal outcomes (Neugebauer, Hoek, & Susser, 1999). Deficits of omega-3 fatty acids have been linked with impaired neurocognition and externalizing behavior (Liu & Raine, 2006; McNamara & Carlson, 2006). The opposite relationship is also supported; increased intake of omega-3 fatty acids has been associated with a variety of positive physical and mental health outcomes (Ruxton, Reed, Simpson, & Millington, 2004), increased brain volume in regions related to memory and emotion regulation (Conklin et al.,2007), and reduction in behavioral problems in children (Raine, Portnoy, Liu, Mahoomed, & Hibbeln, 2015). Studies examining the effect of nutritional supplements have suggested that reducing the amount of sugar consumed by offenders can significantly reduce offending during incarceration (Gesch, Hammond, Hampson, Eves, & Crowder, 2002; Schoenthaler, 1983). Thus, nutritional programs show some promise in reducing antisocial and criminal behavior.

A healthy social environment is also crucial for normative brain development and function. Early adversity and childhood maltreatment have been identified as significant risk factors for both neurobiological and behavioral problems (Mehta et al., 2009; Teicher et al., 2003; Tottenham et al., 2011). A review of maltreatment prevention programs supports the efficacy of nurse-family partnerships and programs that integrate early preschool with parent resources in reducing childhood maltreatment (Reynolds, Mathieson, & Topitzes, 2009). Promoting healthy brain development in utero and in crucial neurodevelopmental periods is likely to reduce externalizing behaviors, as well as other psychopathology.

Knowing that the social context could help to buffer biological risks is promising because it suggests that changing an individual’s environment could mitigate biological criminogenic risk. Rather than providing a reductionist and deterministic perspective of the etiology of criminal behavior, incorporating biological factors in explanations of antisocial/criminal behaviors can highlight the plasticity of the human genome (Walsh & Yun, 2014). They can also provide a more holistic understanding of the etiologies of such behavior. For example, sex differences in heart rate have been found to partially explain the gender gap in crime (Choy, Raine, Venables, & Farrington, 2017). Social interventions that aim to provide an enriched environment can be beneficial for all, but may be particularly important for individuals at higher biological risk for antisocial behavior. While biological explanations of antisocial and criminal behavior are growing, they are best thought of as complementary to current research and theories, and a potential new avenue to target with treatment options.

• Alvarez JA, & Emory E (2006). Executive function and the frontal lobes: A meta-analytic review.Neuropsychology Review, 16,17–42. [PubMed] [Google Scholar]
• Anderson SW, Bechara A, Damasio H, Tranel D, & Damasio AR (1999). Impairment of social and moral behavior related to early damage in human prefrontal cortex. Nature Neuroscience, 2, 1032–1037. [PubMed] [Google Scholar]
• Baker LA, Bezdjian S, & Raine A (2006). Behavioral genetics: The science of antisocial behavior.Law and Contemporary Problems, 69, 7–46. [PMC free article] [PubMed] [Google Scholar]
• Baker LA, Tuvblad C, Reynolds C, Zheng M, Lozano DI, & Raine A (2009). Resting heart rate and the development of antisocial behavior from age 9–14: Genetic and environmental influences. Development and Psychopathology, 21, 939–960. [PMC free article] [PubMed] [Google Scholar]
• Banks SJ, Eddy KT, Angstadt M, Nathan PJ, & Phan KL (2007). Amygdala–frontal connectivity during emotion regulation. Social Cognitive and Affective Neuroscience, 2, 303–312. [PMC free article] [PubMed] [Google Scholar]
• Beach SRH, Brody GH, Todorov AA, Gunter TD, & Philibert RA (2011). Methylation at 5HTT mediates the impact of child sex abuse on women’s antisocial behavior: An examination of the Iowa adoptee sample. Psychosomatic Medicine, 73, 83–87. [PMC free article] [PubMed] [Google Scholar]
• Beaver KM, Wright JP, DeLisi M, Walsh A, Vaughn MG, Boisvert D, & Vaske J (2007). A gene x gene interaction between DRD2 and DRD4 is associated with conduct disorder and antisocial behavior in males. Behavioral and Brain Functions, 3, 30. [PMC free article] [PubMed] [Google Scholar]
• Bechara A, & Damasio AR (2005). The somatic marker hypothesis: A neural theory of economic decision. Games and Economic Behavior, 52, 336–372. [Google Scholar]
• Bjork JM, Chen G, & Hommer DW (2012). Psychopathic tendencies and mesolimbic recruitment by cues for instrumental and passively obtained rewards. Biological Psychology, 89, 408–415. [PMC free article] [PubMed] [Google Scholar]
• Blair RJ (2007). The amygdala and ventromedial prefrontal cortex in morality and psychopathy. Trends in Cognitive Sciences, 11, 387–392. [PubMed] [Google Scholar]
• Boutwell BB, & Beaver KM (2008). A biosocial explanation of delinquency abstention. Criminal Behaviour and Mental Health, 18, 59–74. [PubMed] [Google Scholar]
• Boutwell BB, Menard S, Barnes JC, Beaver KM, Armstrong TA, & Boisvert D (2014). The role of gene-gene interaction in the prediction of criminal behavior. Comprehensive Psychiatry, 55, 483–488. [PubMed] [Google Scholar]
• Brower MC, & Price BH (2001). Advances in neuropsychiatry: Neuropsychiatry of frontal lobe dysfunction in violent and criminal behaviour: A critical review. Journal of Neurology, Neurosurgery & Psychiatry, 71, 720–726. [PMC free article] [PubMed] [Google Scholar]
• Buckholtz JW, Treadway MT, Cowan RL, Woodward ND, Benning SD, Li R,... Smith CE (2010). Mesolimbic dopamine reward system hypersensitivity in individuals with psychopathic traits. Nature Neuroscience, 13, 419–421. [PMC free article] [PubMed] [Google Scholar]
• Burt SA (2009). Are there meaningful etiological differences within antisocial behavior? A metaanalysis. Clinical Psychology Review, 29,163–178. [PubMed] [Google Scholar]
• Byrd AL, & Manuck SB (2014). MAOA, childhood maltreatment, and antisocial behavior: Metaanalysis of a gene-environment interaction. Biological Psychiatry, 75, 9–17. [PMC free article] [PubMed] [Google Scholar]
• Caspi A, McClay J, Moffitt TE, Mill J, Martin J, Craig IW,... Poulton R (2002). Role of genotype in the cycle of violence in maltreated children. Science, 297, 851–854. [PubMed] [Google Scholar]
• Castillo R, Salguero JM, Fernandez-Berrocal P, & Balluerka N (2013). Effects of an emotional intelligence intervention on aggression and empathy among adolescents. Journal of Adolescence, 36, 883–892. [PubMed] [Google Scholar]
• Choy O, Farrington DP, & Raine A (2015). The need to incorporate autonomic arousal in developmental and life-course research and theories. Journal of Developmental and Life-Course Criminology, 1, 189–207. [Google Scholar]
• Choy O, Raine A, & Hamilton RH (2018). Stimulation of the prefrontal cortex reduces intentions to commit aggression: A randomized, double-blind, placebo-controlled, stratified, parallel-group trial. The Journal of Neuroscience, 38, 6505–6512. [PMC free article] [PubMed] [Google Scholar]
• Choy O, Raine A, Venables PH, & Farrington DP (2017). Explaining the gender gap in crime: The role of heart rate. Criminology, 55, 465–487. [Google Scholar]
• Conklin SM, Gianaros PJ, Brown SM, Yao JK, Hariri AR, Manuck SB, & Muldoon MF (2007). Long-chain omega-3 fatty acid intake is associated positively with corticolimbic gray matter volume in healthy adults. Neuroscience Letters, 421, 209–212. [PubMed] [Google Scholar]
• Coutlee CG, & Huettel SA (2012). The functional neuroanatomy of decision making: Prefrontal control of thought and action. Brain Research, 1428C, 3–12. [PMC free article] [PubMed] [Google Scholar]
• Critchley HD (2005). Neural mechanisms of autonomic, affective, and cognitive integration. The Journal of Comparative Neurology, 493, 154–166. [PubMed] [Google Scholar]
• da Cunha-Bang S, Fisher PM, Hjordt LV, Perfalk E, Persson Skibsted A, Bock C,... Knudsen GM (2017). Violent offenders respond to provocations with high amygdala and striatal reactivity. Social Cognitive and Affective Neuroscience, 12(5), 802–810. [PMC free article] [PubMed] [Google Scholar]
• Damasio H, Grabowski T, Frank R, Galaburda AM, & Damasio AR (1994). The return of Phineas Gage: Clues about the brain from the skull of a famous patient. Science, 264, 1102–1105. [PubMed] [Google Scholar]
• Darby RR, Horn A, Cushman F, & Fox MD (2018). Lesion network localization of criminal behavior. Proceedings of the National Academy of Sciences, 115,601–606. [PMC free article] [PubMed] [Google Scholar]
• Davidson RJ, & Irwin W (1999). The functional neuroanatomy of emotion and affective style. Trends in Cognitive Sciences, 3, 11–21. [PubMed] [Google Scholar]
• Delgado-Pastor LC, Perakakis P, Subramanya P, Telles S, & Vila J (2013). Mindfulness (Vipassana) meditation: Effects on P3b event-related potential and heart rate variability. InternationalJournal of Psychophysiology, 90, 207–214. [PubMed] [Google Scholar]
• Delisi M, Beaver KM, Vaughn MG, & Wright JP (2009). All in the family. Criminal Justice and Behavior, 36, 1187–1197. [Google Scholar]
• Dick DM, Adkins AE, & Kuo SI-C (2016). Genetic influences on adolescent behavior. Neuroscience & Biobehavioral Reviews, 70, 198–205. [PMC free article] [PubMed] [Google Scholar]
• Dotterer HL, Hyde LW, Swartz JR, Hariri AR, & Williamson DE (2017). Amygdala reactivity predicts adolescent antisocial behavior but not callous-unemotional traits. Developmental Cognitive Neuroscience, 24, 84–92. [PMC free article] [PubMed] [Google Scholar]
• Eisenberg N (2000). Emotion, regulation, and moral development. Annual Review of Psychology, 51, 665–697. [PubMed] [Google Scholar]
• Ferguson CJ (2010). Genetic contributions to antisocial personality and behavior: A meta-analytic review from an evolutionary perspective. The Journal of Social Psychology, 150, 160–180. [PubMed] [Google Scholar]
• Fergusson DM, Boden JM, & Horwood LJ (2011). MAOA, abuse exposure and antisocial behavior: 30-year longitudinal study. British Journal of Psychiatry, 198, 457–463. [PMC free article] [PubMed] [Google Scholar]
• Ficks CA, & Waldman ID (2014). Candidate genes for aggression and antisocial behavior: A metaanalysis of association studies of the 5HTTLPR and MAOA- uVNTR. Behavior Genetics, 44, 427–444. [PubMed] [Google Scholar]
• Fine C, & Blair RJR (2000). The cognitive and emotional effects of amygdala damage. Neurocase, 6, 435–450. [Google Scholar]
• Focquaert F (2018). Neurobiology and crime: A neuro-ethical perspective. Journal of Criminal Justice. doi: 10.1016/j.jcrimjus.2018.01.001 [CrossRef] [Google Scholar]
• Gao Y, Raine A, & Schug R (2012). Somatic aphasia: Mismatch of body sensations with autonomic stress reactivity in psychopathy. Biological Psychology, 90, 228–233. [PMC free article] [PubMed] [Google Scholar]
• Gao Y, Raine A, Venables PH, Dawson ME, & Mednick SA (2010). Association of poor childhood fear conditioning and adult crime. American Journal of Psychiatry, 167, 56–60. [PubMed] [Google Scholar]
• Gao Y,Tuvblad C, Schell A, Baker L, & Raine A (2015). Skin conductance fear conditioning impairments and aggression: A longitudinal study. Psychophysiology, 52, 288–295. [PMC free article] [PubMed] [Google Scholar]
• Gard AM, Dotterer HL, & Hyde LW (2019). Genetic influences on antisocial behavior: Recent advances and future directions. Current Opinion in Psychology, 27, 46–55. [PubMed] [Google Scholar]
• Gesch CB, Hammond SM, Hampson SE, Eves A, & Crowder MJ (2002). Influence of supplementary vitamins, minerals and essential fatty acids on the antisocial behaviour of young adult prisoners: Randomised, placebo-controlled trial. British Journal of Psychiatry, 181, 22–28. [PubMed] [Google Scholar]
• Geurts DEM, von Borries K, Volman I, Bulten BH, Cools R, &Verkes R-J (2016). Neural connectivity during reward expectation dissociates psychopathic criminals from non-criminal individuals with high impulsive/antisocial psychopathic traits. Social Cognitive and Affective Neuroscience, 11, 1326–1334. [PMC free article] [PubMed] [Google Scholar]
• Gillespie SM, Brzozowski A, & Mitchell IJ (2018). Self-regulation and aggressive antisocial behaviour: Insights from amygdala-prefrontal and heart-brain interactions. Psychology, Crime & Law, 24, 243–257. [Google Scholar]
• Glenn AL, & Raine A (2014). Neurocriminology: Implications for the punishment, prediction and prevention of criminal behaviour. Nature Reviews Neuroscience, 15, 54–63. [PubMed] [Google Scholar]
• Glenn AL, Raine A, Yaralian PS, & Yang Y (2010). Increased volume of the striatum in psychopathic individuals. Biological Psychiatry, 67, 52–58. [PMC free article] [PubMed] [Google Scholar]
• Glenn AL, & Yang Y (2012). The potential role of the striatum in antisocial behavior and psychopathy. Biological Psychiatry, 72, 817–822. [PubMed] [Google Scholar]
• Goldman D, & Rosser AA (2014). MAOA-environment interactions: Results may vary. Biological Psychiatry, 75, 2–3. [PMC free article] [PubMed] [Google Scholar]
• Gregory S, ffytche D, Simmons A, Kumari V, Howard M, Hodgins S, & Blackwood N (2012). The antisocial brain: Psychopathy matters. Archives of General Psychiatry, 69, 962–972. [PubMed] [Google Scholar]
• Hare RD (2017). A person-centered approach to research on the nature and meaning of psychopathy-brain relations. Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, 2,111–112. [PubMed] [Google Scholar]
• Harlow JM (1848). Passage of an iron rod through the head. The Boston Medical and Surgical Journal, 39, 389–393. [Google Scholar]
• Harlow JM (1868). Recovery from the passage of an iron bar through the head. Publications of the Massachusetts Medical Society, 2, 327–347. [Google Scholar]
• Hodzic S, Scharfen J, Ropoll P, Holling H, & Zenasni F (2018). How efficient are emotional intelligence trainings; A meta-analysis. Emotion Review, 10, 138–148. [Google Scholar]
• Hosking JG, Kastman EK, Dorfman HM, Samanez-Larkin GR, Baskin-Sommers A, Kiehl KA, ... Buckholtz JW (2017). Disrupted prefrontal regulation of striatal subjective value signals in psychopathy. Neuron, 95, 221–231.e4. [PMC free article] [PubMed] [Google Scholar]
• Hubbard JA, McAuliffe MD, Morrow MT, & Romano LJ (2010). Reactive and proactive aggression in childhood and adolescence: Precursors, outcomes, processes, experiences, and measurement. Journal of Personality, 78, 95–118. [PubMed] [Google Scholar]
• Hyde LW, Byrd AL, Votruba-Brzal E, Hariri AR, & Manuck SB (2014). Amygdala reactivity and negative emotionality: Divergent correlates of antisocial personality and psychopathy traits in a community sample. Journal of Abnormal Psychology, 123, 214–224. [PMC free article] [PubMed] [Google Scholar]
• Hyde LW, Shaw DS, Murray L, Gard A, Hariri AR, & Forbes EE (2016). Dissecting the role of amygdala reactivity in antisocial behavior in a sample of young, low-income, urban men. Clinical Psychological Science, 4, 527–544. [PMC free article] [PubMed] [Google Scholar]
• Ishikawa SS, Raine A, Lencz T, Bihrle S, & LaCasse L (2001). Autonomic stress reactivity and executive functions in successful and unsuccessful criminal psychopaths from the community. Journal of Abnormal Psychology, 110, 423–432. [PubMed] [Google Scholar]
• Kellermann NP (2013). Epigenetic transmission of Holocaust trauma: Can nightmares be inherited? Israel Journal of Psychiatry and Related Sciences, 50, 33–39. [PubMed] [Google Scholar]
• Kiehl KA, & Hoffman MB (2011). The criminal psychopath: History, neuroscience, treatment, and economics. Jurimetrics, 51, 355–397. [PMC free article] [PubMed] [Google Scholar]
• Kim-Cohen J, Caspi A, Taylor A, Williams B, Newcombe R, Craig IW, & Moffitt TE (2006). Molecular Psychiatry, 11, 903–913. [PubMed] [Google Scholar]
• Knight DC, Smith CN, Cheng DT, Stein EA, & Helmstetter FJ (2004). Amygdala and hippocampal activity during acquisition and extinction of human fear conditioning. Cognitive, affective. & Behavioral Neuroscience, 4, 317–325. [PubMed] [Google Scholar]
• Korponay C, Pujara M, Deming P, Philippi C, Decety J, Kosson DS,... Koenigs M (2017). Impulsive-antisocial dimension of psychopathy linked to enlargement and abnormal functional connectivity of the striatum. Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, 2, 149–157. [PMC free article] [PubMed] [Google Scholar]
• LaBar KS, Gatenby JC, Gore JC, LeDoux JE, & Phelps EA (1998). Human amygdala activation during conditioned fear acquisition and extinction: A mixed-trial fMRI study. Neuron, 20, 937–945. [PubMed] [Google Scholar]
• Latvala A, Kuja-Halkola R, Almqvist C, Larsson H, & Lichtenstein P (2015). A longitudinal study of resting heart rate and violent criminality in more than 700000 men. JAMA Psychiatry, 72,971–978. [PubMed] [Google Scholar]
• Lee TMC, Chan SC, & Raine A (2008). Strong limbic and weak frontal activation in aggressive stimuli in spouse abusers. Molecular Psychiatry, 13, 655–656. [PubMed] [Google Scholar]
• Ling S, Raine A, Gao Y, & Schug R (2018a). The mediating role of emotional intelligence on the autonomic functioning-psychopathy relationship. Biological Psychology, 136, 136–143. [PubMed] [Google Scholar]
• Ling S, Raine A, Yang Y, Schug R, Portnoy J, & Ho M-HR (2018b). Increased frontal lobe volume as a neural correlate of gray-collar offending. Journal of Research in Crime and Delinquency. doi: 10.1177/0022427818802337 [CrossRef] [Google Scholar]
• Liu J, & Raine A (2006). The effect of childhood malnutrition on externalizing behavior. Current Opinion in Pediatrics, 18, 565–570. [PubMed] [Google Scholar]
• Lozier LM, Cardinale EM, VanMeter JW, & Marsh AA (2014). Mediation of the relationship between callous-unemotional traits and proactive aggression by amygdala response to fear among children with conduct problems. JAMA Psychiatry, 71, 627–636. [PMC free article] [PubMed] [Google Scholar]
• Maren S (2001). Neurobiology of Pavlovian fear conditioning. Annual Review of Neuroscience, 24, 897–931. [PubMed] [Google Scholar]
• McNamara RK, & Carlson SE (2006). Role of omega-3 fatty acids in brain development and function: Potential implications for the pathogenesis and prevention of psychopathology. Prostaglandins, Leukotrienes and Essential Fatty Acids, 75, 329–349. [PubMed] [Google Scholar]
• Megreya AM (2015). Emotional intelligence and criminal behavior. Journal of Forensic Sciences, 60, 84–88. [PubMed] [Google Scholar]
• Mehta MA,Golembo NI, Nosarti C,Colvert E, Mota A, Williams SCR,... Sonuga-Barke EJS (2009). Amygdala, hippocampal and corpus callosum size following severe early institutional deprivation: The English and Romanian adoptees study pilot. Journal of Child Psychology and Psychiatry, 50, 943–951. [PubMed] [Google Scholar]
• Meijers J, Harte JM, Meynen G, &Cuijpers P (2017). Differences in executive functioning between violent and non-violent offenders. Psychological Medicine, 47,1784–1793. [PubMed] [Google Scholar]
• Morgan AB, & Lilienfeld SO (2000). A meta-analytic review of the relation between antisocial behavior and neuropsychological measures of executive function. Clinical Psychology Review, 20, 113–136. [PubMed] [Google Scholar]
• Murphy FC, Nimmo-Smith I, & Lawrence AD (2003). Functional neuroanatomy of emotions: A meta-analysis. Cognitive, affective. & Behavioral Neuroscience, 3, 207–233. [PubMed] [Google Scholar]
• Murray L, Shaw DS, Forbes EE, & Hyde LW (2017). Reward-related neural correlates of antisocial behavior and callous-unemotional traits in young men. Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, 2, 346–354. [PMC free article] [PubMed] [Google Scholar]
• Neugebauer R, Hoek HW, & Susser E (1999). Prenatal exposure to wartime famine and development of antisocial personality disorder in early adulthood. Jama, 282, 455–462. [PubMed] [Google Scholar]
• Nitsche MA, & Paulus W (2000). Excitability changes induced in the human motor cortex by weak transcranial direct current stimulation. The Journal of Physiology, 527, 633–639. [PMC free article] [PubMed] [Google Scholar]
• Pardini DA, Raine A, Erickson K, & Loeber R (2014). Lower amygdala volume in men is associated with childhood aggression, early psychopathic traits, and future violence. Biological Psychiatry, 75, 73–80. [PMC free article] [PubMed] [Google Scholar]
• Polaschek DLL, & Skeem JL (2018). Treatment of adults and juveniles with psychopathy In Patrick CJ (Ed.), Handbook of psychopathy, Second Edition (pp. 710–731). New York: Guilford Press. [Google Scholar]
• Portnoy J,& Farrington DP (2015). Resting heart rate and antisocial behavior: An updated systematic review and meta-analysis. Aggression and Violent Behavior, 22, 33–45. [Google Scholar]
• Portnoy J, Raine A, Chen FR, Pardini D, Loeber R, & Jennings JR (2014). Heart rate and antisocial behavior: The mediating role of impulsive sensation seeking. Criminology; An interdisciplinary Journal, 52, 292–311. [Google Scholar]
• Provencal N, & Binder EB (2015). The effects of early life stress on the epigenome: From the womb to adulthood and even before. Experimental Neurology, 268,10–20. [PubMed] [Google Scholar]
• 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, 417–434. [PubMed] [Google Scholar]
• Raine A (2013). The anatomy of violence: The biological roots of crime. New York: Pantheon. [Google Scholar]
• Raine A (2018a). Antisocial personality as a neurodevelopmental disorder. Annual Review of Clinical Psychology, 14, 259–289. [PubMed] [Google Scholar]
• Raine A (2018b). The neuromoral theory of antisocial, violent, and psychopathic behavior. Psychiatry Research. doi: 10.1016/j.psychres.2018.11.025 [PubMed] [CrossRef] [Google Scholar]
• Raine A, Laufer WS, Yang Y, Narr KL, Thompson P, & Toga AW (2012). Increased executive functioning, attention, and cortical thickness in white-collar criminals. Human Brain Mapping, 33, 2932–2940. [PMC free article] [PubMed] [Google Scholar]
• Raine A, Portnoy J, Liu J, Mahoomed T, & Hibbeln JR (2015). Reduction in behavior problems with omega-3 supplementation in children aged 8–16 years: A randomized, double-blind, placebo-controlled, stratified, parallel-group trial. Journal of Child Psychology and Psychiatry, 56, 509–520. [PMC free article] [PubMed] [Google Scholar]
• Raine A, Venables PH, & Williams M (1990). Relationships between central and autonomic measures of arousal at age 15 years and criminality at age 24 years. Archives of General Psychiatry, 47, 1003–1007. [PubMed] [Google Scholar]
• Raine A, & Yang Y (2006). Neural foundations to moral reasoning and antisocial behavior. Social, Cognitive, and Affective Neuroscience, 1, 203–213. [PMC free article] [PubMed] [Google Scholar]
• Reynolds AJ, Mathieson LC, & Topitzes JW (2009). Do early childhood interventions prevent child maltreatment? Child Maltreatment, 14,182–206. [PMC free article] [PubMed] [Google Scholar]
• Rhee SH, & Waldman ID (2002). Genetic and environmental influences on antisocial behavior: A meta-analysis of twin and adoption studies. Psychological Bulletin, 128, 490–529. [PubMed] [Google Scholar]
• Ruxton CHS, Reed SC, Simpson MJA, & Millington KJ (2004). The health benefits of omega-3 polyunsaturated fatty acids: A review of the evidence. Journal of Human Nutrition and Dietetics, 17, 449–459. [PubMed] [Google Scholar]
• Salvatore JE, & Dick DM (2018). Genetic influences on conduct disorder. Neuroscience & Biobehavioral Reviews, 91,91–101. [PMC free article] [PubMed] [Google Scholar]
• Sapolsky RM (2004). The frontal cortex and the criminal justice system. Philosophical Transactions of the Royal Society B: Biological Sciences, 359, 1787–1796. [PMC free article] [PubMed] [Google Scholar]
• Schiffer B, Muller BW, Scherbaum N, Hodgins S, Forsting M, Wiltfang J,... Leygraf N (2011). Disentangling structural brain alterations associated with violent behavior from those associated with substance use disorders. Archives of General Psychiatry, 68, 1039–1049. [PubMed] [Google Scholar]
• Schoenthaler SJ (1983). Diet and crime: An empirical examination of the value of nutrition in the control and treatment of incarcerated juvenile offenders. International Journal of Biosocial Research, 4, 25–39. [Google Scholar]
• Sergerie K, Chochol C, & Armony JL (2008). The role of the amygdala in emotional processing: A quantitative meta-analysis of functional neuroimaging studies. Neuroscience & Biobehavioral Reviews, 32, 811–830. [PubMed] [Google Scholar]
• Sharma N, Prakash O, Sengar KS, Chaudhury S, & Singh AR (2015). The relation between emotional intelligence and criminal behavior: A study among convicted criminals. Industrial Psychiatry Journal, 24, 54–58. [PMC free article] [PubMed] [Google Scholar]
• Sterzer P (2010). Born to be criminal? What to make of early biological risk factors for criminal behavior. American Journal of Psychiatry, 167, 1–3. [PubMed] [Google Scholar]
• Stetler DA, Davis C, Leavitt K,Schriger I, Benson K, Bhakta S,... Bortolato M (2014). Association of low-activity MAOA allelic variants with violent crime in incarcerated offenders. Journal of Psychiatric Research, 58, 69–75. [PMC free article] [PubMed] [Google Scholar]
• Taber-Thomas BC, Asp EW, Koenigs M, Sutterer M, Anderson SW, &Tranel D (2014). Arrested development: Early prefrontal lesions impair the maturation of moral judgement. Brain, 137,1254–1261. [PMC free article] [PubMed] [Google Scholar]
• Teicher MH, Andersen SL, Polcari A, Anderson CM, Navalta CP, & Kim DM (2003). The neu- robiological consequences of early stress and childhood maltreatment. Neuroscience & Biobehavioral Reviews, 27, 33–44. [PubMed] [Google Scholar]
• Tiihonen J, Rautiainen M-R, Ollila HM, Repo-Tiihonen E, Virkkunen M, Palotie A ... Paunio T (2015). Genetic background of extreme violent behavior. Molecular Psychiatry, 20, 786–792. [PMC free article] [PubMed] [Google Scholar]
• Tottenham N, Hare TA, Millner A, Gilhooly T, Zevin JD, & Casey BJ (2011). Elevated amygdala response to faces following early deprivation. Developmental Science, 14, 190–204. [PMC free article] [PubMed] [Google Scholar]
• Umbach R, Raine A, & Leonard NR (2018). Cognitive decline as a result of incarceration and the effects of a CBT/MT intervention: A cluster-randomized controlled trial. Criminal Justice and Behavior, 45, 31–55. [PMC free article] [PubMed] [Google Scholar]
• Vassos E, Collier DA, & Fazel S (2014). Systematic meta-analyses and field synopsis of genetic association studies of violence and aggression. Molecular Psychiatry, 19, 471–477. [PMC free article] [PubMed] [Google Scholar]
• Viding E, Sebastian CL, Dadds MR, Lockwood PL, Cecil CA, De Brito SA, & McCrory EJ (2012). Amygdala response to preattentive masked fear in children with conduct problems: The role of callous-unemotional traits. American Journal of Psychiatry, 169,1109–1116. [PubMed] [Google Scholar]
• Vitiello B, & Stoff DM (1997). Subtypes of aggression and their relevance to child psychiatry. Journal of the American Academy of Child & Adolescent Psychiatry, 36, 307–315. [PubMed] [Google Scholar]
• Wager TD, Waugh CE, Lindquist M, Noll DC, Fredrickson BL, & Taylor SF (2009). Brain mediators of cardiovascular responses to social threat. Neuroimage, 47, 821–835. [PMC free article] [PubMed] [Google Scholar]
• Walsh A, & Yun I (2014). Epigenetics and allostasis: Implications for criminology. Criminal Justice Review, 39, 411–431. [Google Scholar]
• Widom CS, & Brzustowicz LM (2006). MAOA and the “cycle of violence”: childhood abuse and neglect, MAOA genotype, and risk for violent and antisocial behavior. Biological Psychiatry, 60, 684–689. [PubMed] [Google Scholar]
• Woods AJ, Antal A, Bikson M, Boggio PS, Brunoni AR,Celnik P,... Knotkova H (2016). A technical guide to tDCS, and related non-invasive brain stimulation tools. Clinical Neurophysiology, 127, 1031–1048. [PMC free article] [PubMed] [Google Scholar]
• Yang Y, Narr KL, Baker LA, Joshi SH, Jahanshad N, Raine A, & Thompson PM (2015). Frontal and striatal alterations associated with psychopathic traits in adolescents. Psychiatry Research: Neuroimaging, 231, 333–340. [PMC free article] [PubMed] [Google Scholar]
• Yang Y, & Raine A (2009). Prefrontal structural and functional brain imaging findings in anti-social, violent, and psychopathic individuals: A meta-analysis. Psychiatry Research: Neuroimaging, 174,81–88. [PMC free article] [PubMed] [Google Scholar]
• 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, 57,1103–1108. [PubMed] [Google Scholar]
• Yechiam E, Kanz JE, Bechara A, Stout JC, Busemeyer JR, Almaier EM, & Paulsen JS (2008). Neurocognitive deficits related to poor decision-making in people behind bars. Psychonomic Bulletin & Review, 15, 44–51. [PMC free article] [PubMed] [Google Scholar]
• Yuan P, & Raz N (2014). Prefrontal cortex and executive functions in healthy adults: A meta-analysis of structural neuroimaging studies. Neuroscience & Biobehavioral Reviews, 42, 180–192. [PMC free article] [PubMed] [Google Scholar]