Higher subjective social status was also related to less positive feelings in response to the positive and neutral feedback words, though status was unrelated to affective responses to the negative feedback. These data are somewhat consistent with literature showing that individuals from higher socioeconomic status (SES) backgrounds are more likely than lower SES individuals to respond to stressors with extreme emotional distress (Kessler, 1979), as well as some data suggesting that higher-status individuals show greater cortisol responses to acute stress (Gruenewald et al., 2006). It is possible that, because of their relatively greater social standing, individuals reporting higher social status are less accustomed to receiving evaluative feedback and thus experience it as more distressing when they do. However, these in-themoment negative feelings do not appear to translate into get MK-571 (sodium salt) downstream changes in inflammatory activity. Given that physiological and experiential responses to social threat have been shown to have dissociable AG-490 site neural substrates (Wager et al., 2009), it makes sense that biological and self-report responses do not often cohere (Mauss et al., 2005). Much more research is needed to fully understand the complex relationship between social status and psychological vs physiological responses to stress. Data from this study should be interpreted in light of some important limitations. First, all participants in the present sample were female, and it is thus not clear if the findings generalize to males. Second, given that participants were all students at a public university, they have achieved a relatively high level of objective SES, which limits generalizability of the findings to other populations. More research is needed to explore if theseK. A. Muscatell et al.|same neural and inflammatory processes operate at the tails of the objective SES distribution, such as among those living in poverty and/or individuals with extremely high SES. It will also be important for future research to examine if subjective perceptions of social status or objective indicators of SES are stronger predictors of neural and inflammatory responses to social stress, or if there are dissociable neural and physiological stress responses as a function of subjective vs objective SES. Third, given that participants in this study received negative, neutral and positive feedback, we cannot determine if it was specifically the negative feedback that was driving the observed increases in inflammation among those reporting lower social status. It will also be important for future studies to examine if simply being socially evaluated (even if the feedback one receives is positive) is sufficient to increase inflammation among lower subjective status individuals, or if the presence of negative feedback is necessary. Finally, we note that although the effect size for the mediation analysis indicated a medium effect, only the 90 CI did not include 0, possibly due to a small sample size for detecting these sorts of complex relationships between social status, neural activity and physiological responses. More research in larger samples will be needed to replicate this effect, but given that this is the first known study to link social status, neural and inflammatory reactivity data, we believe it is an important first step in exploring the neural mechanisms linking social status and inflammatory responses to stress. Despite these limitations, data from the pres.Higher subjective social status was also related to less positive feelings in response to the positive and neutral feedback words, though status was unrelated to affective responses to the negative feedback. These data are somewhat consistent with literature showing that individuals from higher socioeconomic status (SES) backgrounds are more likely than lower SES individuals to respond to stressors with extreme emotional distress (Kessler, 1979), as well as some data suggesting that higher-status individuals show greater cortisol responses to acute stress (Gruenewald et al., 2006). It is possible that, because of their relatively greater social standing, individuals reporting higher social status are less accustomed to receiving evaluative feedback and thus experience it as more distressing when they do. However, these in-themoment negative feelings do not appear to translate into downstream changes in inflammatory activity. Given that physiological and experiential responses to social threat have been shown to have dissociable neural substrates (Wager et al., 2009), it makes sense that biological and self-report responses do not often cohere (Mauss et al., 2005). Much more research is needed to fully understand the complex relationship between social status and psychological vs physiological responses to stress. Data from this study should be interpreted in light of some important limitations. First, all participants in the present sample were female, and it is thus not clear if the findings generalize to males. Second, given that participants were all students at a public university, they have achieved a relatively high level of objective SES, which limits generalizability of the findings to other populations. More research is needed to explore if theseK. A. Muscatell et al.|same neural and inflammatory processes operate at the tails of the objective SES distribution, such as among those living in poverty and/or individuals with extremely high SES. It will also be important for future research to examine if subjective perceptions of social status or objective indicators of SES are stronger predictors of neural and inflammatory responses to social stress, or if there are dissociable neural and physiological stress responses as a function of subjective vs objective SES. Third, given that participants in this study received negative, neutral and positive feedback, we cannot determine if it was specifically the negative feedback that was driving the observed increases in inflammation among those reporting lower social status. It will also be important for future studies to examine if simply being socially evaluated (even if the feedback one receives is positive) is sufficient to increase inflammation among lower subjective status individuals, or if the presence of negative feedback is necessary. Finally, we note that although the effect size for the mediation analysis indicated a medium effect, only the 90 CI did not include 0, possibly due to a small sample size for detecting these sorts of complex relationships between social status, neural activity and physiological responses. More research in larger samples will be needed to replicate this effect, but given that this is the first known study to link social status, neural and inflammatory reactivity data, we believe it is an important first step in exploring the neural mechanisms linking social status and inflammatory responses to stress. Despite these limitations, data from the pres.
