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Socioeconomic status (SES), often conceptualized as income, education, or occupation, is associated with risk for disease morbidity and psychopathology. Recent research has focused on the potential biological mechanisms linking lower SES and poor outcomes; much of this work has examined the relationship between SES and markers of systemic inflammation. The strength of the estimated association between SES and inflammatory markers varies widely across individual studies. Thus, we used meta-analytic techniques to quantify the magnitude of this relationship. To accomplish this, PubMed and PsycINFO were searched for papers that reported on SES and two commonly measured systemic inflammatory markers, C-reactive protein (CRP) and interleukin-6 (IL-6). Peer-reviewed, empirical papers conducted in non-patient populations were included. Data from 43 papers (N = 111,156) reporting a total of 63 relevant effect sizes were included in analyses. SES, broadly defined, was significantly associated with both levels of CRP (Z = 0.12; 95% CI, 0.09–0.16) and IL-6 (Z = 0.15; 95% CI, 0.12–0.18); individuals with lower SES showed higher levels of systemic inflammation. Subanalyses demonstrated that studies operationalizing SES as either levels of income or educational attainment also found significant associations with both CRP and IL-6. Moderator analyses revealed that effect sizes varied based on sample characteristics and analysis approaches. Lower SES is associated with significantly elevated levels of inflammatory markers of disease risk. Thus, pro-inflammatory pathways are likely an important mechanism translating socioeconomic inequalities into mental and physical health disparities.

Although social withdrawal is a prominent symptom of sickness, the mechanisms associated with this behavioral change remain unclear. In animals, the amygdala is a key neural region involved in sickness-induced social withdrawal. Consistent with this, in humans, heightened amygdala activity to negative social cues is associated with social avoidance tendencies. Based on these findings, we investigated whether an experimental inflammatory challenge selectively increased amygdala activity to socially threatening images as well as whether this activity related to feelings of social disconnection. Thirty-nine participants were randomly assigned to receive either placebo or low-dose endotoxin, which increases inflammatory activity. Pro-inflammatory cytokines were assessed at 7 hourly time points via blood draws; self-reported feelings of social disconnection and physical sickness symptoms were assessed hourly as well. Two hours post-injection, participants underwent an fMRI procedure to assess amygdala reactivity during the presentation of socially threatening images (fear faces) as well as non-socially threatening images (guns), socially non-threatening images (happy faces), and non-social, non-threatening images (household objects). Endotoxin led to greater amygdala activity in response to socially threatening vs. all other types of images. No such differences were found for placebo participants. Additionally, increased amygdala activity in endotoxin participants during the viewing of socially vs. non-socially threatening images was associated with increased feelings of social disconnection. These findings highlight the amygdala as a neural region that may be important for sickness-induced social withdrawal. The implications of amygdalar involvement in sickness-induced social withdrawal are discussed. ► We investigated neural responses to social stimuli after an inflammatory challenge. ► Inflammation led to greater amygdala to socially threatening vs. other images. ► Amygdala activity was positively correlated with feelings of social disconnection. ► Amygdala activity may be important for sickness-induced social withdrawal.

Dysregulation of the immune system is one potential mechanism by which acute stress may contribute to downstream disease etiology and psychopathology. Here, we tested the role of β-adrenergic signaling as a mediator of acute stress-induced changes in immune cell gene expression. In a randomized, double-blind, and placebo-controlled trial, 90 healthy young adults (44% female) received a single 40 mg dose of the β-blocker propranolol (n = 43) or a placebo (n = 47) and then completed the Trier Social Stress Test (TSST). Pre- and post-stress blood samples were assayed for prespecified sets of pro-inflammatory and antiviral/antibody gene transcripts. Analyses revealed increased expression of both inflammatory and antiviral/antibody-related genes in response to the TSST, and these effects were blocked by pre-treatment with propranolol. Bioinformatics identified natural killer cells and dendritic cells as the primary cellular context for transcriptional upregulation, and monocytes as the primary cellular carrier of genes downregulated by the TSST. These effects were in part explained by acute changes in circulating cell types. Results suggest that acute psychosocial stress can induce an “acute defense” molecular phenotype via β-adrenergic signaling that involves mobilization of natural killer cells and dendritic cells at the expense of monocytes. This may represent an adaptive response to the risk of acute injury. These findings offer some of the first evidence in humans that β-blockade attenuates psychosocial stress-induced increases in inflammatory gene expression, offering new insights into the molecular and immunologic pathways by which stress may confer risks to health and well-being.

Abstract Roughly 20 years of functional magnetic resonance imaging (fMRI) studies have investigated the neural correlates underlying engagement in social cognition (e.g. empathy and emotion perception) about targets spanning various social categories (e.g. race and gender). Yet, findings from individual studies remain mixed. In the present quantitative functional neuroimaging meta-analysis, we summarized across 50 fMRI studies of social cognition to identify consistent differences in neural activation as a function of whether the target of social cognition was an in-group or out-group member. We investigated if such differences varied according to a specific social category (i.e. race) and specific social cognitive processes (i.e. empathy and emotion perception). We found that social cognition about in-group members was more reliably related to activity in brain regions associated with mentalizing (e.g. dorsomedial prefrontal cortex), whereas social cognition about out-group members was more reliably related to activity in regions associated with exogenous attention and salience (e.g. anterior insula). These findings replicated for studies specifically focused on the social category of race, and we further found intergroup differences in neural activation during empathy and emotion perception tasks. These results help shed light on the neural mechanisms underlying social cognition across group lines.

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.

Socioeconomic status (SES)-related health disparities persist for numerous chronic diseases, with lower-SES individuals exhibiting greater risk of morbidity and mortality compared to their higher-SES counterparts. One likely contributor is disparities in health messaging efforts, which are currently less effective for motivating health behavior change among those lower in SES. Drawing on communication neuroscience and social neuroscience research, we describe a conceptual framework to improve health messaging effectiveness in lower SES communities. The framework is based on evidence that health-message-induced activity in the ventral striatum (VS) and subdivisions of the medial pre-frontal cortex (MPFC) predicts behavior change. Additionally, we draw from social neuroscience work showing that activity in these regions during valuation and the processing of self-related vs. social information, differs as a function of SES. Bringing together these previously disparate lines of work, we argue that health messages emphasizing the benefits to close others (vs. the self) of engaging in behavior change will be more effective among lower SES individuals. We also outline a research agenda based on our framework. Ultimately, we hope that this framework utilizing a “brain-as-predictor” approach generates novel insights about the neural underpinnings of message-induced behavior change among lower SES individuals, and helps to close the gap in SES-based health disparities by harnessing the power of neuroimaging.

Loneliness is a distressing state indicating that one’s basic need for social connection is not being met. In an effort to satisfy the need for social connection, loneliness may increase the processing of social cues and desire to connect with others. Yet the neural substrates that contribute to the drive for increased connection in response to loneliness are not known. The ventral striatum (VS), previously shown to increase in response to craving food and other rewarding stimuli, may contribute to “social craving” when one is lonely. That is, the VS may track one’s ‘hunger’ for reconnection much as it tracks hunger for food. To examine this, participants reported on their feelings of loneliness before undergoing an fMRI scan where they viewed cues of potential social reconnection (images of a close other). Consistent with the hypothesis that loneliness stems from an unmet need for connection, loneliness was associated with reduced feelings of connection with the close other. Furthermore, greater reported loneliness was associated with increased VS activity to viewing a close other (vs stranger). Results extend the current literature by showing that lonely individuals show increased activity in reward-related regions to their closest loved ones, possibly reflecting an increased desire for social connection.

Adolescence is a sensitive period for sociocultural development in which facets of social identity, including social status and race, become especially salient. Despite the heightened importance of both social status and race during this developmental period, no known work has examined how individual differences in social status influence perceptions of race in adolescents. Thus, in the present study, we investigated how both subjective social status and objective socioeconomic status (SES) influence neural responses to race. Twenty-three Mexican American adolescents (15 females; mean age = 17.22 years) were scanned using functional magnetic resonance imaging while they viewed Black and White faces in a standard labeling task. Adolescents rated their subjective social status in US society, while their parents responded to questions about their educational background, occupation, and economic strain (objective SES). Results demonstrated a negative association between subjective social status and neural responses in the amygdala, fusiform face area, and medial prefrontal cortex when adolescents viewed Black (relative to White) faces. In other words, adolescents with lower subjective social status showed greater activity in neural regions involved in processing salience, perceptual expertise, and thinking about the minds of others when they viewed images of Black faces, suggesting enhanced salience of race for these youth. There was no relationship between objective SES and neural responses to the faces. Moreover, instructing participants to focus on the gender or emotion expression on the face attenuated the relationship between subjective social status and neural processing of race. Together, these results demonstrate that subjective social status shapes the way the brain responds to race, which may have implications for psychopathology.

The current research explored the neural mechanisms linking social status to perceptions of the social world. Two fMRI studies provide converging evidence that individuals lower in social status are more likely to engage neural circuitry often involved in ‘mentalizing’ or thinking about others' thoughts and feelings. Study 1 found that college students' perception of their social status in the university community was related to neural activity in the mentalizing network (e.g., DMPFC, MPFC, precuneus/PCC) while encoding social information, with lower social status predicting greater neural activity in this network. Study 2 demonstrated that socioeconomic status, an objective indicator of global standing, predicted adolescents' neural activity during the processing of threatening faces, with individuals lower in social status displaying greater activity in the DMPFC, previously associated with mentalizing, and the amygdala, previously associated with emotion/salience processing. These studies demonstrate that social status is fundamentally and neurocognitively linked to how people process and navigate their social worlds.

Abstract Experiences within one’s social environment shape neural sensitivity to threatening and rewarding social cues. However, in racialized societies like the USA, youth from minoritized racial/ethnic backgrounds can have different experiences and perceptions within neighborhoods that share similar characteristics. The current study examined how neighborhood disadvantage intersects with racial/ethnic background in relation to neural sensitivity to social cues. A racially diverse (59 Hispanic/Latine, 48 White, 37 Black/African American, 15 multi-racial and 6 other) and primarily low to middle socioeconomic status sample of 165 adolescents (88 female; Mage = 12.89) completed a social incentive delay task while undergoing functional magnetic resonance imaging (fMRI) scanning. We tested for differences in the association between neighborhood disadvantage and neural responses to social threat and reward cues across racial/ethnic groups. For threat processing, compared to White youth, neighborhood disadvantage was related to greater neural activation in regions involved in salience detection (e.g. anterior cingulate cortex) for Black youth and regions involved in mentalizing (e.g. temporoparietal junction) for Latine youth. For reward processing, neighborhood disadvantage was related to greater brain activation in reward, salience and mentalizing regions for Black youth only. This study offers a novel exploration of diversity within adolescent neural development and important insights into our understanding of how social environments may ‘get under the skull’ differentially across racial/ethnic groups.