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Psychobiology of Violence

The document discusses three main factors related to the psychobiology of violence: psychophysiology, the brain, and genetics. It provides details on how blunted autonomic functioning and abnormalities in areas like the prefrontal cortex, amygdala, and striatum may increase antisocial and criminal behavior.
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0% found this document useful (0 votes)
37 views20 pages

Psychobiology of Violence

The document discusses three main factors related to the psychobiology of violence: psychophysiology, the brain, and genetics. It provides details on how blunted autonomic functioning and abnormalities in areas like the prefrontal cortex, amygdala, and striatum may increase antisocial and criminal behavior.
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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Psychobiolog

y of Violence
MPCL
Forensic Psychology
Three Main Factors
1. Psychophysiology
2. Brain
3. Genetics
Psychophysiology
• 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, &
Psychophysiology
• 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
Psychophysiology
• 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).
Psychophysiology
• 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
Brain
• 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
Prefrontal Cortex (PFC)
• 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
Prefrontal Cortex (PFC)
• 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.
Prefrontal Cortex (PFC)
• 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
Amygdala
• 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).
Amygdala
• 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
Striatum
• 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
Striatum
• 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
Neuromoral theory of anti-social
behaviour
• 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
Neuromoral theory of anti-social
behaviour
• 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
genetics
• 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).
genetics
• 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
genetics
• 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
genetics
• 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 &

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