Why social pain can live on: Different neural mechanisms are associated with reliving social and physical pain

Although social and physical pain recruit overlapping neural activity in regions associated with the affective component of pain, the two pains can diverge in their phenomenology. Most notably, feelings of social pain can be re-experienced or relived, even when the painful episode has long passed, whereas feelings of physical pain cannot be easily relived once the painful episode subsides. Here, we observed that reliving social (vs. physical) pain led to greater self-reported re-experienced pain and greater activity in affective pain regions (dorsal anterior cingulate cortex and anterior insula). Moreover, the degree of relived pain correlated positively with affective pain system activity. In contrast, reliving physical (vs. social) pain led to greater activity in the sensory-discriminative pain system (primary and secondary somatosensory cortex and posterior insula), which did not correlate with relived pain. Preferential engagement of these different pain mechanisms may reflect the use of different top-down neurocognitive pathways to elicit the pain. Social pain reliving recruited dorsomedial prefrontal cortex, often associated with mental state processing, which functionally correlated with affective pain system responses. In contrast, physical pain reliving recruited inferior frontal gyrus, known to be involved in body state processing, which functionally correlated with activation in the sensory pain system. These results update the physical-social pain overlap hypothesis: while overlapping mechanisms support live social and physical pain, distinct mechanisms guide internally-generated pain. © 2015 Meyer et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Sex Differences in the Effect of Inflammation on Subjective Social Status: A Randomized Controlled Trial of Endotoxin in Healthy Young Adults.

It has been established that inflammation leads to a variety of changes in social experience, but one area of social experience that has been overlooked is subjective social status. Furthermore, given sex differences in the relationship between inflammation and social status, males may be more sensitive to inflammation-induced changes in social status. However, no previous studies in humans have examined this possibility. In the present study, healthy young participants (n = 115) were randomly assigned to receive either endotoxin, an experimental inflammatory challenge, or placebo. Participants reported their subjective social status at baseline (prior to injection), and approximately 2 h later (time of peak inflammatory response for the endotoxin group). Results, using ANCOVA analyses, indicated that males exposed to endotoxin, but not females, reported lower levels of subjective social status at the peak of inflammatory response (vs. placebo). These results suggest that males may be more sensitive to the effects of inflammation in certain social domains, such as perceived social status. Clinical Trial Registration: www.ClinicalTrials.gov, identifier NCT01671150

In Sickness and in Health: The Co-Regulation of Inflammation and Social Behavior

Although it has commonly been assumed that the immune system and the processes that govern social behavior are separate, non-communicating entities, research over the past several decades suggests otherwise. Considerable evidence now shows that inflammatory processes and social behavior are actually powerful regulators of one another. This review first summarizes evidence that inflammatory processes regulate social behavior, leading to characteristic changes that may help an individual navigate the social environment during times of sickness. Specifically, this review shows that inflammation: (1) increases threat-related neural sensitivity to negative social experiences (eg, rejection, negative social feedback), presumably to enhance sensitivity to threats to well-being or safety in order to avoid them and (2) enhances reward-related neural sensitivity to positive social experiences (eg, viewing close others and receiving positive social feedback), presumably to increase approach-related motivation towards others who might provide support and care during sickness. Next, this review summarizes evidence showing that social behavior also regulates aspects of inflammatory activity, preparing the body for situations in which wounding and infection may be more likely (social isolation). Here, we review research showing: (1) that exposure to social stressors increases proinflammatory activity, (2) that individuals who are more socially isolated (ie, lonely) show increased proinflammatory activity, and (3) that individuals who are more socially isolated show increased proinflammatory activity in response to an inflammatory challenge or social stressor. The implications of the co-regulation of inflammation and social behavior are discussed

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When Less is More: Mindfulness Predicts Adaptive Affective Responding to Rejection Via Reduced Prefrontal Recruitment

Social rejection is a distressing and painful event that many people must cope with on a frequent basis. Mindfulness—defined here as a mental state of receptive attentiveness to internal and external stimuli as they arise, moment-to-moment—may buffer such social distress. However, little research indicates whether mindful individuals adaptively regulate the distress of rejection—or the neural mechanisms underlying this potential capacity. To fill these gaps in the literature, participants reported their trait mindfulness and then completed a social rejection paradigm (Cyberball) while undergoing functional magnetic resonance imaging. Approximately 1 hour after the rejection incident, participants reported their level of distress during rejection (i.e. social distress). Mindfulness was associated with less distress during rejection. This relation was mediated by lower activation in the left ventrolateral prefrontal cortex during the rejection incident, a brain region reliably associated with the inhibition of negative affect. Mindfulness was also correlated with less functional connectivity between the left ventrolateral prefrontal cortex and the bilateral amygdala and the dorsal anterior cingulate cortex, which play a critical role in the generation of social distress. Mindfulness may relate to effective coping with rejection by not over-activating top-down regulatory mechanisms, potentially resulting in more effective long-term emotion-regulation

Preliminary Evidence That CD38 Moderates the Association of Neuroticism on Amygdala-Subgenual Cingulate Connectivity.

CD38 genetic variation has been associated with autism spectrum disorders and social anxiety disorder, which may result from CD38's regulation of oxytocin secretion. Converging evidence has found that the rs3796863 A-allele contributes to increased social sensitivity compared to the CC genotype. The current study examined the moderating role of CD38 genetic variants (rs3796863 and rs6449182) that have been associated with enhanced (or reduced) social sensitivity on neural activation related to neuroticism, which is commonly elevated in individuals with social anxiety and depression. Adults (n = 72) with varying levels of social anxiety and depression provided biological samples for DNA extraction, completed a measure of neuroticism, and participated in a standardized emotion processing task (affect matching) while undergoing fMRI. A significant interaction effect was found for rs3796863 x neuroticism that predicted right amygdala-subgenual anterior cingulate cortex (sgACC) functional connectivity. Simple slopes analyses showed a positive association between neuroticism and right amygdala-sgACC connectivity among rs3796863 A-allele carriers. Findings suggest that the more socially sensitive rs3796863 A-allele may partially explain the relationship between a known risk factor (i.e. neuroticism) and promising biomarker (i.e. amygdala-sgACC connectivity) in the development and maintenance of social anxiety and depression