Neural representations of vicarious rewards are linked to interoception and prosocial behaviour.

Every day we constantly observe other people receiving rewards. Theoretical accounts posit that vicarious reward processing might be linked to people's sensitivity to internal body states (interoception) and facilitates a tendency to act prosocially. However, the neural processes underlying the links between vicarious reward processing, interoception, and prosocial behaviour are poorly understood. Previous research has linked vicarious reward processing to the anterior cingulate gyrus (ACCg) and the anterior insula (AI). Can we predict someone's propensity to be prosocial or to be aware of interoceptive signals from variability in how the ACCg and AI process rewards? Here, participants monitored rewards being delivered to themselves or a stranger during functional magnetic resonance imaging. Later, they performed a task measuring their willingness to exert effort to obtain rewards for others, and a task measuring their propensity to be aware and use interoceptive respiratory signals. Using multivariate similarity analysis, we show that people's willingness to be prosocial is predicted by greater similarity between self and other representations in the ACCg. Moreover, greater dissimilarity in self-other representations in the AI is linked to interoceptive propensity. These findings highlight that vicarious reward is linked to bodily signals in AI, and foster prosocial tendencies through the ACCg.

Neural and Cognitive Signatures of Guilt Predict Hypocritical Blame.

A common form of moral hypocrisy occurs when people blame others for moral violations that they themselves commit. It is assumed that hypocritical blamers act in this manner to falsely signal that they hold moral standards that they do not really accept. We tested this assumption by investigating the neurocognitive processes of hypocritical blamers during moral decision-making. Participants (62 adult UK residents; 27 males) underwent functional MRI scanning while deciding whether to profit by inflicting pain on others and then judged the blameworthiness of others' identical decisions. Observers (188 adult U.S. residents; 125 males) judged participants who blamed others for making the same harmful choice to be hypocritical, immoral, and untrustworthy. However, analyzing hypocritical blamers' behaviors and neural responses shows that hypocritical blame was positively correlated with conflicted feelings, neural responses to moral standards, and guilt-related neural responses. These findings demonstrate that hypocritical blamers may hold the moral standards that they apply to others.

Prosocial behavior is associated with transdiagnostic markers of affective sensitivity in multiple domains.

Prosocial behaviors-actions that benefit others-fundamentally shape our interpersonal interactions. Psychiatric disorders have been suggested to be related to prosocial disturbances, which may underlie many of their social impairments. However, broader affective traits, present to different degrees in both psychiatric and healthy populations, also have been linked to variability in prosociality. Therefore, it is unclear to what extent prosocial variability is explained by specific psychiatric disorders relative to broad affective traits. Using a computational, transdiagnostic approach in two online studies, we found that participants who reported being more affectively reactive across a broad cluster of traits manifested greater frequencies of prosocial actions in two different contexts: They reported being more averse to harming others for profit, and they were more willing to exert effort to benefit others. These findings help illuminate the profile of prosociality across psychiatric conditions as well as the architecture of prosocial behavior in healthy individuals. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Effort shapes social cognition and behaviour: A neuro-cognitive framework.

Theoretical accounts typically posit that variability in social behaviour is a function of capacity limits. We argue that many social behaviours are goal-directed and effortful, and thus variability is not just a function of capacity, but also motivation. Leveraging recent work examining the cognitive, computational and neural basis of effort processing, we put forward a framework for motivated social cognition. We argue that social cognition is demanding, people avoid its effort costs, and a core-circuit of brain areas that guides effort-based decisions in non-social situations may similarly evaluate whether social behaviours are worth the effort. Thus, effort sensitivity dissociates capacity limits from social motivation, and may be a driver of individual differences and pathological impairments in social cognition.

Racial bias in neural response to others' pain is reduced with other-race contact.

Observing the pain of others has been shown to elicit greater activation in sensory and emotional areas of the brain suggested to represent a neural marker of empathy. This modulation of brain responses to others' pain is dependent on the race of the observed person, such that observing own-race people in pain is associated with greater activity in the anterior cingulate and bilateral insula cortices compared to other-race people. Importantly, it is not known how this racial bias to pain in other-race individuals might change over time in new immigrants or might depend on the level and quality of contact with people of the other-race. We investigated these issues by recruiting Chinese students who had first arrived in Australia within the past 6 months to 5 years and assessing their level of contact with other races across different social contexts using comprehensive rating scales. During fMRI, participants observed videos of own-race/other-race individuals, as well as own-group/other-group individuals, receiving painful or non-painful touch. The typical racial bias in neural responses to observed pain was evident, whereby activation in the anterior cingulate cortex (ACC) was greater for pain in own-race compared to other-race people. Crucially, activation in the anterior cingulate to pain in other races increased significantly with the level of contact participants reported with people of the other race. Importantly, this correlation did not depend on the closeness of contact or personal relationships, but simply on the overall level of experience with people of the other race in their every-day environment. Racial bias in neural responses to others' pain, as a neural marker of empathy, therefore changes with experience in new immigrants at least within 5 years of arrival in the new society and, crucially, depends on the level of contact with people of the other race in every-day life contexts.

Intergroup relationships do not reduce racial bias in empathic neural responses to pain.

Perceiving the pain of others activates similar neural structures to those involved in the direct experience of pain, including sensory and affective-motivational areas. Empathic responses can be modulated by race, such that stronger neural activation is elicited by the perception of pain in people of the same race compared with another race. In the present study, we aimed to identify when racial bias occurs in the time course of neural empathic responses to pain. We also investigated whether group affiliation could modulate the race effect. Using the minimal group paradigm, we assigned participants to one of two mixed-race teams. We examined event-related potentials from participants when viewing members of their own and the other team receiving painful or non-painful touch. We identified a significant racial bias in early ERP components at N1 over frontal electrodes, where Painful stimuli elicited a greater negative shift relative to Non-Painful stimuli in response to own race faces only. A long latency empathic response was also found at P3, where there was significant differentiation between Painful and Non-Painful stimuli regardless of Race or Group. There was no evidence that empathy-related brain activity was modulated by minimal group manipulation. These results support a model of empathy for pain that consists of early, automatic bias towards own-race empathic responses and a later top-down cognitive evaluation that does not differentiate between races and may ultimately lead to unbiased behaviour.

Racial bias in neural empathic responses to pain.

Recent studies have shown that perceiving the pain of others activates brain regions in the observer associated with both somatosensory and affective-motivational aspects of pain, principally involving regions of the anterior cingulate and anterior insula cortex. The degree of these empathic neural responses is modulated by racial bias, such that stronger neural activation is elicited by observing pain in people of the same racial group compared with people of another racial group. The aim of the present study was to examine whether a more general social group category, other than race, could similarly modulate neural empathic responses and perhaps account for the apparent racial bias reported in previous studies. Using a minimal group paradigm, we assigned participants to one of two mixed-race teams. We use the term race to refer to the Chinese or Caucasian appearance of faces and whether the ethnic group represented was the same or different from the appearance of the participant' own face. Using fMRI, we measured neural empathic responses as participants observed members of their own group or other group, and members of their own race or other race, receiving either painful or non-painful touch. Participants showed clear group biases, with no significant effect of race, on behavioral measures of implicit (affective priming) and explicit group identification. Neural responses to observed pain in the anterior cingulate cortex, insula cortex, and somatosensory areas showed significantly greater activation when observing pain in own-race compared with other-race individuals, with no significant effect of minimal groups. These results suggest that racial bias in neural empathic responses is not influenced by minimal forms of group categorization, despite the clear association participants showed with in-group more than out-group members. We suggest that race may be an automatic and unconscious mechanism that drives the initial neural responses to observed pain in others.