Neurobiology of empathy and callousness: Implications for the development of antisocial behavior

Abstract

Information on the neurobiology of empathy and callousness provides clinicians an opportunity to develop sophisticated understanding of mechanisms underpinning antisocial behavior and its counterpart, moral decision making. This paper provides an integrated in-depth review of hormones (e.g., peripheral steroid hormones like cortisol) and brain structures (e.g., insula, anterior cingulate cortex, and amygdala) implicated in empathy, callousness and psychopathic-like behavior. The overarching goal of this paper is to relate these hormones and brain structures to moral decisionmaking. This review will begin in the brain, but will then integrate information about biological functioning in the body, specifically stress-reactivity. Our aim is to integrate understanding of neural processes with hormones like cortisol, both of which have demonstrated relationships to empathy, psychopathy, and antisocial behavior. The review proposes neurobiological impairments in individuals who display little empathy are not necessarily due to a reduced ability to understand the emotions of others. Instead, evidence suggests individuals who show little arousal to the distress of others likewise show decreased physiological arousal to their own distress; one manifestation of reduced stress reactivity may be a dysfunction in empathy which supports psychopathic-like constructs (e.g., callousness). This integration will assist in the development of objective methodologies that can inform and monitor treatment interventions focused on decreasing antisocial behavior.Keywords moral decision making; psychopathy; empathy; callousness The purpose of this paper is to review and integrate the neurobiological underpinnings of empathy and callousness to promote understanding of mechanisms behind moral decisionmaking and, conversely, the development of antisocial behavior. This paper is divided into two main sections. We will begin in the brain, reviewing a triad of neurocircuitry involved in empathy as well as the unique neural signature of callousness and antisocial behavior. This section will highlight (a) brain areas that show overlapping activation across empathy-and callousness-focused investigations, and then (b) neural processes that are unique to callousness. Much of this circuitry has strong reciprocal connections with peripheral physiology, including stress-reactive hormones like cortisol. The second section will review evidence that cortisol and the hypothalamic-pituitary-adrenal (HPA) axis is (a) connected with the neurocircuitry NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript involved with empathy and/or callousness and (b) correlated with empathy or prosocial behavior as well as callous or antisocial behavior. The point of combining neural and peripheral physiology is to suggest that impairments in moral decision-making in psychopathic individuals may not directly involve impairments in the ability to feel emotions of another. The mechanism may be more basic, involving general difficulties in respondi...

Testosterone, Cortisol and Empathy: Evidence for the Dual-Hormone Hypothesis

“…Why this positive relationship between testosterone and empathy was restricted to individuals with a greater HPA output remains to be clarified. However, as suggested by other authors (Shirtcliff et al 2009), one explanation is that higher cortisol levels would mirror a state of mild arousal and internal distress that aid empathy.…”

“…2 Trait empathy as a function of basal testosterone and cortisol levels in men and women. When basal cortisol was low, basal testosterone was negatively related to empathy Reduced basal HPA activity is associated with fearlessness, reduced sensitivity to punishment and threat (Van Honk et al 2003), and some aspects of aggression (Van Goozen et al 2007;Shirtcliff et al 2009;but see, Van Bokhoven et al 2005), whereas high cortisol levels are associated with anxiety (Brown et al 1996) and submissive behavior (i.e. social withdrawal and inhibition; Kagan et al 1988;Goldsmith and Lemery 2000;Klimes-Dougan et al 2001), but also with higher empathy (reviewed in Shirtcliff et al 2009).…”

“…Future research on the dual hormone hypothesis and empathy should consider using alternative measures of empathy, such as, for example, the Movie for the Assessment of Social Cognition (MASC), a test in which participants have to infer mental states and feelings of four people filmed while having dinner (Dziobek et al 2006). Future research should also consider other hormonal measures, for example, cortisol reactivity to stress instead of baseline cortisol, as recent evidence indicates that stress cortisol may modulate prosocial behavior (reviewed in Shirtcliff et al 2009 andPreston 2014).…”

Associations between glucocorticoids and sociality across a continuum of vertebrate social behavior

“…Even though the existence of actual empathy in nonhuman species is controversial, social responsiveness plays a key role in social behavior in all species inhabiting complex social groups. Because GCs may enhance vigilance and responsiveness to external stimuli in general, it is not surprising that empathy correlates positively with hormonal stress responsiveness in humans (Shirtcliff et al., 2009). This suggests the possibility that individuals with elevated HPA‐axis activity in cooperative species are more responsive to the state of other group members, potentially enhancing their cooperative capability.…”

Brain imaging research on psychopathy: Implications for punishment, prediction, and treatment in youth and adults

“…In contrast, the more robust finding to date in this area is amygdala hypoactivity when processing emotional or empathy-inducing stimuli in psychopathic-like children and adolescents. Impaired empathy and/or facial expression recognition are both risk factors for antisocial behavior (Shirtcliff et al, 2009;Blair, 2003) and also bear on the core features of callous-unemotional traits. What has not been addressed in the literature is whether amygdala under-responsivity predisposes to callous-unemotional traits, or alternatively whether these traits result in down-regulation of the amygdala and have a different etiology.…”