Biological correlates of antagonism

Biological correlates of antagonism

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Julia McDonald, Edelyn Verona Department of Psychology, University of South Florida, Tampa, FL, United States

Introduction and theoretical foundations In 1848, Phineas Gage was working on a railroad when an explosion turned a railway spike into a projectile that impaled Gage through his skull. Gage survived; however, his personality was purportedly altered as a result of damage to his prefrontal cortex (Damasio, Grabowski, Frank, Galaburda, & Damasio, 1994). After the accident, “Gage was no longer Gage,” showing behaviors described as “fitful, irreverent, and grossly profane, showing little deference for his fellows” (Harlow, 1868, pp. 13–14). And with that, the explosion of a metal rod ushered the field of neuroscience into the modern era. While the idea that personality is inextricably linked to biology is by no means a new one, most contemporary theories of personality psychology, including the FiveFactor Model (FFM; Costa & McCrae, 1992), have not been mapped onto biological systems (Paris, 2000). This lack of data is unfortunate when considering that certain personality traits, such as antagonism (the low pole of FFM agreeableness), are key predictors of behaviors of particular concern for society, such as violence and crime (Skeem, Miller, Mulvey, Tiemann, & Monahan, 2005). A clearer understanding of the psychobiological processes associated with the antagonistic personality is essential to understanding etiology and maintenance factors. High agreeableness is an obviously adaptive social strategy: empathy, straightforwardness, and cooperation are all related to increased social support, successful parenting, and conflict resolution (Nettle, 2006). Nonetheless, evolutionary theorists argue that the opposite pole, antagonism, is also an advantageous strategy for resource allocation and genetic reproduction (Buss, 1996). Studies have shown that aspects of antagonism are related to career success, successful short-term mating strategies, social dominance, and other traits that serve to protect and promote the interest of the person (Spurk, Keller, & Hirschi, 2016; Zeigler-Hill & Hobbs, 2017). As such, trait antagonism has persisted, as have the biological/genetic signatures associated with this trait dimension. Indeed, antagonistic traits are heritable, with estimates from twin studies ranging from 33% to 51% of the variance in antagonism accounted for by genes (for review see Bouchard & Loehlin, 2001). Antagonism, as conceptualized within FFM, and measured by trait inventories like the NEO Personality Inventory—Revised (NEO-PI-R; Costa & McCrae, 1992), is comprised of separate but related facets of trust (versus distrust), straightforwardness The Handbook of Antagonism. https://doi.org/10.1016/B978-0-12-814627-9.00006-2 © 2019 Elsevier Inc. All rights reserved.

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(versus manipulation), altruism (versus self-centeredness), compliance (versus oppositionality), modesty (versus arrogance), and tender-mindedness (versus callousness). The individual facets are likely associated with distinct etiological factors and behavioral manifestations. For example, low physiological arousal allows antagonistic individuals to perform under high-stress situations (Hall & Benning, 2006), lack of responsiveness to the distress of others allows self-centered individuals to focus on their own needs before worrying about others (Shirtcliff et al., 2009), and hypervigilance to threat serves to protect distrustful individuals from being taken advantage of (Riedl & Javor, 2012). This chapter aims to provide an integrated review of the biological mechanisms associated with combinations of facets of antagonism. We aim to integrate findings from hormones, genes, peripheral physiology (e.g., bodily reactivity to emotional stimuli) as well as neurocircuitry (e.g., brain structures and systems) to identify common patterns characterizing a general tendency toward antagonism, as well as distinct biological processes across the facets.

Unconcern for others and low empathy (callousness, self-centeredness) One of the defining features of antagonism includes lower levels of caring or empathic concern for others, captured by the antagonism facets of callousness and selfcenteredness. Constructs associated with trait callousness include youth callous and unemotional (CU) traits (Frick & White, 2008); the affective traits of adult psychopathy (lack of emotional depth/empathy/remorse and shallow affect, as assessed by the Psychopathy Checklist-Revised; PCL-R, Hare, 2003); coldheartedness (Berg, Hecht, Latzman, & Lillienfeld, 2015); and the “meanness” dimension of the triarchic model of psychopathy (Patrick, Fowles, & Krueger, 2009). Self-centeredness overlaps conceptually with callousness in terms of its characteristic low level of concern for others, egocentricity, exploitiveness, and greedy behaviors. Self-centeredness is implicated in narcissistic personality disorder (Miller, Gentile, Wilson, & Campbell, 2013), Machiavellianism (Lynam et al., 2011), as well as several psychopathic traits (egocentrism, shallow affect, and reckless disregard for the safety of others; Hare, 2003). Callous and egocentric traits show moderate to high heritability ( Jang, Livesley, & Vernon, 1996; Jang, McCrae, Angleitner, Riemann, & Livesley, 1998). Results from a range of studies of youth CU traits and psychopathy have shown that callousness is linked to high levels of genetic (20%–71%) and nonshared environmental influence (54%–80%), without contribution from shared environment (Larsson et al., 2007; Viding, Jones, Frick, Moffitt, & Plomin, 2008). Callousness, as measured by the NEO-PI-R mirrors this research ( Jang et al., 1996, 1998). Research on selfcenteredness has repeatedly found a major influence of the nonshared environment (64%–80%; Jang et al., 1996, 1998), but less consistent estimates for the genetic and environmental influences (Bouchard & Loehlin, 2001). Together these studies suggest that while both self-centeredness and callousness are influenced by the nonshared environment, callousness is likely more heritable than self-centeredness.

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Less is known about the individual genes involved in callousness and selfcenteredness, although there is growing work in the area. For example, although the short allele of the serotonin linked polymorphic region of the serotonin transporter gene (5-HTTLPR) has been implicated in impulsivity and emotional excesses (Ficks & Waldman, 2014; Sadeh, Javdani, Jackson, & Reynolds, 2010), the long allele of 5-HTTLPR has received attention in regard to affective deficits in psychopathy (Sadeh et al., 2010; Sadeh, Verona, & Javdani, 2013). This double dissociation makes sense, given that the long allele of 5-HTTLPR has been linked to both reduced stress reactivity and emotional responding (Glenn, 2011), such as lower resting activation of the amygdala (Canli, Congdon, Gutknecht, Constable, & Lesch, 2005) and reduced stress system activity (Gotlib, Joormann, Minor, & Hallmayer, 2008) relative to the other variants of 5-HTTLPR. The neurohormone oxytocin has been linked to attachment, pair bonding, social support, and prosocial behavior (Kumsta & Heinrichs, 2013), and thus deficits in oxytocin functioning are implicated in callousness and self-centeredness. In one study, intranasal administrations of oxytocin increased altruism (opposite pole of self-centeredness), with participants donating more money to charities with a social framing (i.e., helping people in need) than nature conservation (i.e., saving the rainforest; Marsh et al., 2015). Further, genetic variation in the oxytocin receptor (OXTR) gene, and related single-nucleotide polymorphisms on that gene (SNPs rs1042778, rs53576, and rs2254298; Thompson, Hurd, & Crespi, 2013), have been linked to empathy, social bonding, and social cue recognition (Gong et al., 2017), and more recently with the affective (callous) facet of psychopathy (Verona, Murphy, & Bresin, 2018). Furthermore, a recent epigenetics study found that high levels of both CU traits and OXTR methylation interacted to produce increased decoupling of amygdala and frontal regions (Aghajani et al., 2018). Functionally, this decoupling may affect processing involved in decoding and integrating socioaffective information. Together, this set of studies suggests reduced social sensitivity among persons high on callous/egocentric features of antagonism. Consistent with this, studies across levels of analysis indicate that persons high on callous and self-centered traits show reduced stress reactivity, fear, and defensive responding. Studies of hormonal systems relevant to threat responsivity have found that CU traits and affective features of psychopathy are related to reduced levels of basal cortisol (Loney, Butler, Lima, Counts, & Eckel, 2006), as well as blunted cortisol reactivity (O’Leary, Loney, & Eckel, 2007). Further, affective features of psychopathy and CU traits are associated with reduced reactivity in skin conductance and heart rate to emotionally evocative conditions (Fung et al., 2005; Lorber, 2004), particularly unpleasant ones, as well as reduced resting heart rate and skin conductance (Lorber, 2004). Similarly, decades of research have shown that individuals high on psychopathic traits (particularly interpersonal and affective traits) and youth with CU traits do not show a normal startle reflex potentiation in response to aversive stimuli (Vaidyanathan, Hall, Patrick, & Bernat, 2011). These studies provide compelling evidence that behavioral manifestations relevant to callous/self-centered traits are associated with reduced defensive responding.

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Findings of reduced stress reactivity are in line with research on the structure and function of the limbic system, with reduced volume and activity of the amygdala consistently linked to abnormal affective processing observed in psychopaths (Weber, Habel, Amunts, & Schneider, 2008). Neuroimaging studies have linked reduced amygdala functioning to psychopathy and CU traits (Blair, Jones, Clark, & Smith, 1997), callousness (Shirtcliff et al., 2009), and low empathy (Bernhardt & Singer, 2012). Notably, biological indicators of emotional responding such as the fearpotentiated startle (Angrilli et al., 1996) and hormone levels such as cortisol (van Stegeren et al., 2007), which show deficient levels in callousness, are modulated by amygdala reactivity. At the level of larger brain networks, self-centeredness and callousness have been associated with dysfunction of the salience network (Shirtcliff et al., 2009). This network includes the anterior cingulate cortex (ACC) and the insula (Menon & Uddin, 2010) and has been implicated in generating physiological arousal and promoting attention in response to alerting stimuli. Individuals high in traits relevant to callousness and self-centeredness (e.g., affective traits of psychopathy) show reduced insula and ACC activation, including in response to signals of distress or pain experienced by others (Blair, 2013; Decety, Chen, Harenski, & Kiehl, 2013). However, narcissism (which is a behavioral manifestation relevant to self-centeredness, but also captured by arrogant/manipulative facets of antagonism, see later) has been associated with increased activation of the right anterior insula during evaluation of negative emotional images (Fan et al., 2011), a region often implicated in representations of the self. Thus, there is evidence of heightened salience network activation in narcissism-related self-centeredness, particularly in response to perceived threats to self ( Jankowiak-Siuda & Zajkowski, 2013), which may distinguish it from other low empathy-related constructs. In summary, the literature supports that callousness, and self-centeredness to a lesser extent, are manifestations of a particular underlying pattern of biology, which is heritable with mostly nonshared environmental influence. The physiological literature indicates a pattern of reduced sensitivity to social and emotional cues, which coincides with the “low fear” hypothesis (Lykken, 1995) of psychopathic/CU traits. This hypothesis characterizes callousness as the inability to properly process aversive or emotional stimuli, leading to the reduced subjective experience of fear and concomitant failures to avoid fear-provoking situations, recognize fear in others, and correct inappropriate behavior.

Hostile orientation toward others (oppositionality, distrust) Another set of widely studied features of antagonism include oppositionality and distrustful traits—both reflecting a general hostile orientation toward others. Behavioral manifestations of oppositionality include lack of cooperation, combativeness, and willingness to fight back, with extreme manifestations represented in many of the disorders characterized by antisocial behavior and aggression

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( Jones, Miller, & Lynam, 2011). Distrust represents tendencies toward feelings of persecution and viewing others in a hostile light, manifested in vulnerable narcissism (Miller et al., 2016) and paranoid personality disorder (Samuel & Widiger, 2008). While these behavioral manifestations are linked by a shared underlying association to trait antagonism, some are also thought to be influenced by lack of conscientiousness (Kotov et al., 2017) and/or neuroticism ( Jones et al., 2011). As with callousness, oppositionality and distrust seem to be moderately heritable (30%–52%; Hiraishi, Yamagata, Shikishima, & Ando, 2008; Jang et al., 1996; Rhee & Waldman, 2002; Tuvblad, Bezdjian, Raine, & Baker, 2014). Distrust, as measured by the NEO-PI-R, shows the largest environmental influences of all antagonism facets, with estimates of the amount of nonshared environmental influence highly consistent across studies (64%–70%; Jang et al., 1996; Jang, Livesley, Angleitner, Riemann, & Vernon, 2002). In contrast, shared environment only seems relevant to the expression of oppositionality (specifically, antisocial behavior; 14%–41% in boys; Larsson et al., 2007; Viding, Blair, Moffitt, & Plomin, 2005). Together, these studies suggest that oppositionality/distrust have heritable components but are highly influenced by the environment. Candidate genes relevant to oppositionality have been most widely studied in relation to antisocial behavior. The low activity variant of monoamine oxidase A (MAOA) gene has been consistently linked to expressions of aggression, antisocial behavior, and violence across studies (Ficks & Waldman, 2014). Similarly, the short allele of the serotonin promoter variant 5-HTTLPR is related to increased antisocial behavior, aggression, and antisocial and impulsive facets psychopathy (Ficks & Waldman, 2014; Sadeh et al., 2010, 2013). The latter gene variant represents a possible etiological distinction between callousness and oppositionality: the long allele of 5-HTTLPR is related to blunted affect and decreased physiological reactivity (implicated in callousness), whereas the short allele of 5-HTTLPR is related to increased physiological reactivity in response to stressful or emotional stimuli (implicated in oppositionality, as reviewed later), respectively (Glenn, 2011). Although persons can be simultaneously high on both callousness and oppositionality, different etiological pathways (e.g., blunted affect or stress reactivity/dysregulation) can result in the same combined phenotype. In terms of environmental influences, more replicable findings show that the relationships between the MAOA or 5-HTTLPR gene variants and antisocial behavior or aggression are much stronger among persons with higher levels of childhood adversity or maltreatment (e.g., Kim-Cohen et al., 2006). Hormone systems regulating testosterone, oxytocin, and cortisol have been jointly implicated in oppositionality and distrust. High levels of basal testosterone have been observed in persons high on oppositionality or distrust, especially in studies of oppositionality-related aggression traits (Geniole, Busseri, & McCormick, 2013). Testosterone may also promote distrust, with one study finding that the administration of the steroid hormone testosterone decreased perceptions of trust during a facial trustworthiness evaluation task (Bos, Terburg, & Van Honk, 2010). This result could be attributable to testosterone’s inhibition of oxytocin (Huber, Veinante, & Stoop, 2005); indeed, distrust shows negative associations with oxytocin (Domes et al., 2007). Importantly, oxytocin release seems to suppress cortisol reactivity and

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amygdala activation, suggesting that enhanced stress reactivity underlies distrust tendencies, and combined with high testosterone, implicates higher threat sensitivity across oppositionality/distrust. Inconsistent with this conceptualization, however, low levels of basal cortisol (indicative of underarousal at rest) have been reported in persons with aggressive, oppositional, and antisocial behavior (Lopez-Duran, Olson, Hajal, Felt, & Vazquez, 2009; McBurnett, Lahey, & Rathouz, 2000), but the findings here have been somewhat mixed (Alink et al., 2008). The idea of higher threat reactivity among those with antisocial/aggressive behaviors would also contradict evidence of blunted resting autonomic activity (Lorber, 2004; Portnoy & Farrington, 2015), especially electrodermal activity (Crider, 2008; Lorber, 2004). However, evidence from various literatures supports the idea that oppositionality (e.g., aggressive, violent, or antisocial behavior problems) is marked by threat sensitivity, including increased autonomic reactivity, especially in response to provocation (Pham, Philippot, & Rime, 2000) and increased processing of evocative stimuli (Lorber, 2004). Whereas callousness is characterized by both low baseline arousal and low stress reactivity (and blunted cortisol reactivity), oppositionality reflects low baseline arousal but heightened stress reactivity (and testosterone). This again illustrates that distinct developmental pathways may be involved in the manifestation of antagonism traits. This pattern of increased threat reactivity is also observed in neuroimaging work, with increased activation of the amygdala to evocative stimuli in oppositionality and distrust (Engell, Haxby, & Todorov, 2007), with some null findings (Matthys, Vanderchuren, & Schutter, 2013). Other research indicates that enhanced emotional processing is combined with dysfunctions in cognitive control. That is, studies show deficits in structure and functioning of the prefrontal cortex among those with distrustful (Riedl & Javor, 2012) and oppositional traits (e.g., conduct and oppositional defiant disorder, psychopathy, antisocial/aggressive behavior; Matthys et al., 2013 Patrick, 2014). Studies using eventrelated potential techniques have consistently found that the P300 (the component thought to index cognitive control) is reduced among individuals with antisocial traits (Gao & Raine, 2009), and these cognitive control deficits are thought to uniquely characterize antisocial behavior, rather than the affective traits associated with callousness (Hicks et al., 2007). Lastly, activation of the insula has been associated with abnormal expressions of interpersonal trust. For example, patients with focal damage to the insula were found to display continued trust for a dishonest stranger (Belfi, Koscik, & Tranel, 2015), and increased insula activation has been associated with heightened sensitivity toward betrayal (Aimone, Houser, & Weber, 2014). These studies suggest that heightened insula activation is related to distrust. In fact, distrust has been associated with both increased activation (Dimoka, 2010) and gray matter volume of the insula in nonclinical samples (Haas, Ishak, Anderson, & Filkowski, 2015). In the sense that the insula is part of the salience network, chronic activation can bias the cognitive and affective systems toward viewing many benign situations as indications of potential threats, subsequently resulting in increased likelihood for hostility and distrust (Verona & Bresin, 2015; Young et al., 2017).

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Together, evidence suggests that oppositionality/distrust are characterized by a pattern of low baseline arousal but a chronically activated threat response system, coupled with difficulty downregulating impulses (reduced cognitive control). While this biobehavioral profile may be adaptive in dangerous environments, it also predisposes individuals toward hostility, aggression, and antisocial behaviors. The increased autonomic and amygdala reactivity and functioning of the insula represent a possible biological distinction between oppositionality/distrust and callousness/egocentricity. Whereas the former is undergirded by heightened sensitivity toward potential threat, the latter is insensitive to potential signs of threat.

Social dominance and deception (manipulation, arrogance) The last major set of antagonism traits include manipulation and arrogance—both representing strategies for deceiving and dominating others. Antagonistic manipulation involves a duplicitous interpersonal style that utilizes flattery or deception to control others. This facet has been linked to Machiavellianism (O’Boyle, Forsyth, Banks, Story, & White, 2015); deceitfulness in antisocial personality disorder; and the interpersonal manipulation seen in psychopathy, narcissism, and borderline personality disorder (Lynam, 2012). Antagonistic arrogance is marked by apparent confidence, boastfulness, and belief of one’s own superiority and is observed in grandiose features of psychopathy and grandiose narcissism (Miller et al., 2016), as well as histrionic personality disorder (Samuel & Widiger, 2008). These facets have less biological research, and behavioral manifestations of Machiavellianism and narcissism are also considerably driven by other FFM domains including high extraversion, high neuroticism, and low conscientiousness; therefore biological findings based on these phenotypes may be driven only partly by antagonism (O’Boyle et al., 2015). The research on the heritability of these traits has suggested a typical combination of genetic and environmental influences. Heritability studies that have utilized the NEO-PI-R ( Jang et al., 1996, 1998) have found that manipulation and arrogance are attributed mainly to the nonshared environment (53%–75%). However, whereas manipulation seems to be also driven by additive genetics (25%–47%), arrogance seems to be instead driven in part by shared family environment (26%–33%). These results are consistent with research on the Dark Triad (psychopathy, narcissism, and Machiavellianism), which reflect extremes in both arrogant and manipulative behaviors. Research suggests dark traits are driven mostly by genetic (31%–64%) and nonshared environmental factors (30%–41%), although Machiavellianism was also influenced by the shared environment (39%) (Vernon, Villani, Vickers, & Harris, 2008). Like other facets of antagonism, arrogant/manipulative traits (at least as manifested in narcissism) have also been linked to hormones such as testosterone and cortisol. One study investigating the Dark Triad (measured using the Short Dark Triad measure; Jones & Paulhus, 2014) found that grandiose narcissism (but not Machiavellianism or psychopathy) was associated with increased basal levels of testosterone and cortisol, suggesting a link between these hormones and propensities toward social

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domination as well as a sensitivity toward social esteem and status (Pfattheicher, 2016). Grandiose narcissism, in particular, has been associated with increased cortisol reactivity in response to interpersonal stressors and perceived threats to the self (Edelstein, Yim, & Quas, 2010). This is consistent with the idea that social evaluation and status elicits a strong threat response for individuals with narcissism. Finally, testosterone levels have been found to underlie the relationship between grandiose narcissism and aggression (Lobbestael, Baumeister, Fiebig, & Eckel, 2014), suggesting that higher levels of basal testosterone may predispose narcissistic individuals toward aggressive behavior. However, others argue that the testosterone-cortisol ratio is most important, specifically low levels of cortisol combined with high levels of testosterone (Terburg, Morgan, & van Honk, 2009). In a related vein, narcissism has been associated with heightened activation of the salience network, particularly increased right anterior insula activity, the region implicated in representation of the self (Fan et al., 2011). These data are consistent with theoretical interpretations of the narcissistic interpersonal style in regard to sensitivity to perceived threat to their ego, resulting in a variety of interpersonal strategies such as manipulation and arrogance as a means of self-protection (Baumeister, Smart, & Boden, 1996). Indeed, alterations in neural circuits related to the self are observed in narcissism, with evidence of weakened connectivity between the regions of the brain involved in processing of self-relevant stimuli (medial-prefrontal cortex) and reward (ventral-striatum) (Chester, Lynam, Powell, & DeWall, 2015). This physiological disconnect between representations of the self and reward would be consistent with self-regulatory theories of narcissism (Morf & Rhodewalt, 2001). Specifically, for narcissists, arrogance and external validation seeking serves as a regulatory strategy to compensate for deficits in deriving an intrinsic sense of self-worth. While the arrogance associated with narcissism involves heightened reactivity and preoccupation with representations of the self, manipulative tendencies may relate to decreased sensitivity to the emotional consequences of deceiving others (e.g., anxiety, guilt, sympathy). For example, the brain has been shown to adapt to dishonesty, such that with continued lying, the amygdala response dampens to the negative feeling associated with preparing to tell a lie (Garrett, Lazzaro, Ariely, & Sharot, 2016). This suggests that habituation to deception may actually cause reduced amygdala activation, although more research is needed to determine the causal nature of the relationship. Further, the interpersonal-affective facet of psychopathy has been associated with lower activation of the amygdala and enhanced activation of the dorsolateral prefrontal cortex during an emotionrecognition task, suggesting that these individuals rely less on emotional centers of the brain for processing emotional information (Gordon, Baird, & End, 2004). Consistent with this, studies consistently find that intentionally deceiving someone in an experimental deception task is associated with increased activity in the prefrontal cortex among a nonclinical sample (Abe, Suzuki, Mori, Itoh, & Fujii, 2007). Studies have associated pathological lying (measured using the PCL-R) with increased prefrontal white matter (Yang et al., 2007) and Machiavellianism with increased prefrontal cortex gray matter volume (Verbeke et al., 2011).

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Machiavellianism was also found to be associated with increased activation of the dorsolateral prefrontal cortex during a laboratory Trust game but only during conditions that required cooperation (Bereczkei et al., 2015). This suggests that for individuals with Machiavellian traits, cooperative social interactions require more cognitive effort, possibly because these interactions involve weighing the pros and cons of exploiting another person for personal gain. Collectively, these findings suggest that manipulation, in particular, relates to deficits in the emotional processing regions of the brain, in combination with increased prefrontal involvement in processing cues. In summary, the arrogant and manipulative facets of antagonism have been less researched in the context of biological studies. These traits characterize individuals with an increased propensity toward social dominance and sensitivity toward social esteem/status, coupled with an ease with which to use deception and flattery to achieve one’s goals. These tendencies are associated with at least two physiological profiles: the increased vigilance to threats to self (e.g., hyperactive salience network, increased basal testosterone and cortisol) observed in arrogance/narcissism, and the decreased reliance on emotional processing and more effortful control during deception. Whereas arrogance involves a biased preoccupation with the self, manipulation involves more calculated and cold processing of social cues to determine the most advantageous option for the self. The somewhat discordant biological findings across arrogance and manipulation may mirror the distinct social style differences observed between these traits (e.g., boastfulness versus deceit), but which all represent behavioral strategies for achieving/maintaining dominance over others.

Conclusions The primary aim of this chapter was to summarize the existing literature on the biological correlates of trait antagonism. Few studies have directly investigated antagonism as measured by FFM inventories, so we have included relevant studies from various fields including psychopathology, personality/social psychology, behavioral economics, neuroscience, and criminology. The evidence suggests that antagonism is characterized by specific alterations in processes involved in bonding and attachment, social and emotional processing, and responding to threat cues. Importantly, our review suggests that different combinations of traits result in different manifestations at the behavioral level. We argue that the heterogeneity in antagonistic phenotypes is mirrored in their physiological manifestations, and the latter can help understand the social behavior in the former. Antagonistic facets share tendencies toward lower social cooperation and decreased social bonding and a general insensitivity to social cues. This is substantiated biologically by reductions in oxytocin system activity observed across facets of antagonism (specifically, callousness, self-centeredness, distrust, and manipulation). While more research is needed to establish causality, it appears that deficits in levels of oxytocin may contribute to the decreased social bonding and affiliation associated

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with antagonism. When this generalized lower social bonding combines with mechanisms associated with specific facets, distinct biobehavioral manifestations of antagonism can be identified. As one example, the relative insensitivity to threat and distress cues and altered emotional processing shown by self-centered and callous persons can result in reduced empathy and reduced ability to recognize inappropriate behavior or avoid dangerous situations. There is evidence of a somewhat similar biological profile in persons showing deceit and manipulation, although the reduced processing of emotional information is combined with higher reliance on cognitive centers during interpersonal interactions. At the same time, arrogant narcissism is associated with heightened reactivity to threats to or representations of the self. This combined pattern makes it easier for individuals high on arrogance and manipulation to deceive and exploit others, especially when they detect threats to status. Relative to other antagonistic facets, the biological profile of oppositionality/distrust shows a fairly distinct pattern of heightened threat response and poor downregulation of impulses. These individuals are not reluctant to respond to frustrating or threatening situations with a hostile confrontation and have difficulty inhibiting these reactions in inappropriate circumstances. This tendency would result in frequent negative interpersonal interactions, which would then only serve to reinforce their continued mistrust and resentment of others. This review serves to motivate future work in this area to improve our understanding of the neurobiology related to antagonism. First, future research should use the FFM to specifically study the biological correlates of antagonistic personality traits. This would reduce the ambiguity by addressing whether biological correlates are actually being driven by antagonism or by some other FFM domain. Second, as the literature on the biology of trait antagonism continues to grow, researchers should consider environmental and contextual factors that influence the expression of antagonistic traits (e.g., gender role). Third, mapping FFM antagonism traits to biobehavioral correlates can help inform treatment by identifying subtypes of individuals most amenable to certain intervention strategies. For instance, for individuals with primarily oppositional and mistrustful traits, treatment aimed at adjusting automatic negative reactions might be most useful; whereas for primarily callous or self-centered individuals, intervention might include learning to detect and understand the emotions of others. Finally, there are a few caveats to note to avoid common misunderstandings that often accompany interpreting biological research. The study of biological factors does not rule out the importance of environmental influences. Rather, the ultimate cause of behavior is due to a complex interaction between both biology and environmental/ social factors. Differences in brain and biology should not be taken to be fixed or innate; the environment has a powerful and lifelong influence on physiology. The goal of biological psychology is to gain a better understanding of how biological factors combine with environmental influences to promote behavior. As such, a truly biological perspective incorporates both nature and nurture and acknowledges that this dynamic interplay occurs throughout the lifetime.

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