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Objectives: To investigate whether childhood adversity exacerbates the relationship between sleep restriction and inflammation., Methods: Participants (N = 46) were randomly assigned to an experimental sleep restriction group (n = 25) or a night of typical sleep (n = 21). Participants provided a dried blood spot sample the morning before and after the experimental night., Results: A significant interaction emerged between childhood adversity and group assignment on C-reactive protein (CRP) after the experimental night (Beta = -0.02, SE = 0.01, P = .03, 95% CI: -0.05, -0.002). Sleep restriction resulted in an increase in CRP at high levels of childhood adversity (+1 SD; Effect = -0.57, SE = 0.15, P< .001; 95% CI: -0.87, -0.26) but not low levels of childhood adversity (Effect = -0.08, SE = 0.10, P = .40; 95% CI: -0.29, 0.12)., Conclusion: Childhood adversity may amplify the effect of sleep loss on markers of inflammation., (Copyright © 2022 National Sleep Foundation. Published by Elsevier Inc. All rights reserved.)

Background: Previous research documents an association between adverse childhood experiences (ACEs) and immune system inflammation. High chronic inflammation is believed to be one biological pathway through which childhood adversity may affect health into adulthood. The Blackfeet tribal community has high rates of childhood trauma and community members are disproportionately affected by inflammatory diseases., Purpose: To investigate whether belonging to the tribal community may moderate the relationship between childhood trauma and immune system inflammation in the Blackfeet tribal community., Methods: In a sample of 90 adults residing on the Blackfeet reservation, we measured ACEs belonging to the tribal community and two markers of immune system inflammation, interleukin-6 (IL-6) and C-reactive protein (CRP)., Results: We found that independent of age, gender, annual income, body mass index, and depressive symptoms, belonging to the tribal community and ACEs interacted to predict levels of both IL-6 and CRP (B= -.37, t[81] = -3.82, p < .001, R2 change = .07 and B = -.29, t[81] = -2.75, p = .01, R2 change = .08, respectively). The association between ACEs and markers of immune system inflammation was statistically significant for community members who reported low levels of belonging to the community., Conclusions: The findings of this study have important implications for intervention research seeking to reduce risk for inflammatory diseases for at-risk populations. Fostering stronger connections to the larger tribal community may positively affect risk for inflammatory diseases. Future work should examine the behavioral and psychosocial pathways through which stronger connections to community may confer health benefits., (© Society of Behavioral Medicine 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Inflammatory reactivity to acute laboratory stress is thought to reflect individual differences in responsivity to environmental stressors and may confer future health risk. To characterize this response, we conducted a meta-analysis of 34 studies that measured circulating inflammatory markers and 15 studies that measured stimulated production of inflammatory markers before and after exposure to laboratory challenge. Results showed significant stress-related increases in circulating interleukin (IL)-1β (d=0.66, p<0.001), IL-6 (d=0.35, p<0.001), IL-10 (d=0.69, p<0.001), and tumor necrosis factor(TNF)-α (d=0.28, p<0.001), but not IL-1ra, IL-2, interferon-γ, or C-reactive protein. There were sufficient data to assess the time course of IL-6, IL-1β, and TNF-α reactivity. IL-6 increased from baseline to measures taken 40-50, 60-75, 90, and 120min following stress, with the largest effect at 90min post-stress (d=0.70, p<0.001). IL-1β increased from baseline to 20-30, 40-50, and 60-70min following stress, with the largest effect between 40 and 50min post-stress (d=0.73, p=0.02). For TNF-α, there was a significant increase from baseline to 31-50min post stress (d=0.44, p=0.01), but not at later times. There was no difference in magnitude of IL-6 reactivity as a function of type of stress (social-evaluative versus other). For stimulated inflammatory markers, results showed stress-related increases in IL-1β when measured 20-120min post-stress (d=1.09, p<0.001), and in IL-4 and interferon-γ when measured 0-10min post stressor (d=-0.42, p<0.001 and d=0.47, p<0.001). These results extend findings from a prior meta-analysis (Steptoe et al., 2007) to show reliable increases in circulating IL-6, IL-1β, IL-10 and TNF-α and stimulated IL-1β, IL-4 and interferon-γ in response to acute stress. It is possible that these responses contribute to associations between exposure to life challenges and vulnerability to inflammatory disease., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Objective: Systemic inflammation is thought to be a biological mediator between social relationship quality and premature mortality. Empirical work has yielded mixed support for an association of social relationship variables with systemic inflammation, perhaps due to methodological limitations. To date, research in this literature has focused on global perceptions of social relationships, with limited attention to the covariance of characteristics of daily social interactions with inflammation. Here, we examine whether daily interactions, as assessed by ecological momentary assessment (EMA), associate with peripheral markers of inflammation among midlife and older adults., Methods: Global social support and integration were measured using the Interpersonal Support Evaluation List (ISEL) and the Social Network Index (SNI), respectively, in older adults from the Pittsburgh Healthy Heart Project (PHHP), and in middle-aged adults from the Adult Health and Behavior Project-II (AHAB-II). Using time-sampled EMA, we assessed the proportion of the day spent in positive and negative social interactions. Systemic markers of inflammation were interleukin (IL)-6 and C-reactive protein (CRP)., Results: Global measures of support and integration did not associate with inflammation in either sample. In older adults, relative frequency of total positive interactions, those with close others (i.e. spouse, friends, family), and those with coworkers predicted lower concentrations of IL-6 in fully adjusted models, accounting for age, sex, race, education, BMI, smoking and alcohol. In middle-aged adults, relative frequency of positive interactions with close others was also inversely associated with IL-6 level and relative frequency of negative marital interactions was unexpectedly inversely associated with CRP level., Conclusions: Characteristics of daily social interactions among midlife and older adults associate with markers of systemic inflammation that are known to predict risk for cardiovascular disease. Ambulatory measures may better capture health-relevant social processes in daily life than retrospective, global self-report measures., (Published by Elsevier Inc.)

Low socioeconomic status (SES) during childhood confers risk for adverse health in adulthood. Accumulating evidence suggests that this may be due, in part, to the association between lower childhood SES and higher levels of pro-inflammatory cytokines. Drawing from literature showing that low childhood SES predicts exaggerated physiological reactivity to stressors and that lower SES is associated with a more communal, socially attuned orientation, we hypothesized that inflammatory reactivity would be more greatly affected by cues of social support among individuals whose childhood SES was low than among those whose childhood SES was high. In two studies, we found that individuals with lower subjective childhood SES exhibited greater reductions in pro-inflammatory cytokine reactivity to a stressor in the presence of a supportive figure (relative to conditions with an unsupportive or neutral figure). These effects were independent of current SES. This work helps illuminate SES-based differences in inflammatory reactivity to stressors, particularly among individuals whose childhood SES was low., (© The Author(s) 2015.)

In response to social-evaluative threat induced in the laboratory, lower (compared to higher) subjective social class of a participant predicts greater increases in the inflammatory cytokine interleukin-6 (IL-6). In spite of the interpersonal nature of social-evaluation, little work has explored whether characteristics of the evaluator shape physiological responses in this context. In the current study, in a sample of 190 college students (male=66), we explored whether one's subjective social class interacts with the perceived social class of an evaluator to predict changes in Oral Mucosal Transudate (OMT) IL-6 in response to the Trier Social Stress Test (TSST). Participants were randomly assigned to be the speaker or the evaluator. Extending past work, we found that while speakers low in subjective social class consistently respond with strong increases in IL-6 regardless of their perception of their evaluator's social class, speakers high in subjective social class responded with greater increases in IL-6 when their evaluator was perceived as high social class compared to when they were perceived as low social class. This finding highlights the importance of perceptions of the evaluator in informing inflammatory responses to a social-evaluative task., (Copyright © 2015 Elsevier B.V. All rights reserved.)

In response to social-evaluative threat induced in the laboratory, lower (compared to higher) subjective social class of a participant predicts greater increases in the inflammatory cytokine interleukin-6 (IL-6). In spite of the interpersonal nature of social-evaluation, little work has explored whether characteristics of the evaluator shape physiological responses in this context. In the current study, in a sample of 190 college students (male=66), we explored whether one's subjective social class interacts with the perceived social class of an evaluator to predict changes in Oral Mucosal Transudate (OMT) IL-6 in response to the Trier Social Stress Test (TSST). Participants were randomly assigned to be the speaker or the evaluator. Extending past work, we found that while speakers low in subjective social class consistently respond with strong increases in IL-6 regardless of their perception of their evaluator's social class, speakers high in subjective social class responded with greater increases in IL-6 when their evaluator was perceived as high social class compared to when they were perceived as low social class. This finding highlights the importance of perceptions of the evaluator in informing inflammatory responses to a social-evaluative task.

This research independently manipulated two potential attenuators of stereotype threat - reappraisal of anxiety and test framing - to explore their independent and combined effects. Female participants took a difficult math exam that was described as gender-biased or gender-fair and were told that anxious arousal could positively impact performance or were given no information regarding arousal. Levels of the cytokine Interleukin-6 (IL-6), an immune marker of inflammation, were measured in oral mucosal transudate (OMT) both before and after the exam. Our findings indicate that directing reappraisal of physiological arousal attenuated increases in IL-6 across test framing conditions, and was especially effective under stereotype threat (i.e., gender-biased test condition). Reappraisal also mapped onto better test performance in the threat condition. Together, these findings provide insight into the unique and interactive effects of two situational interventions meant to reduce stereotype threat, indexed here by both physiological and performance-based correlates of threat.

BackgroundSubjective social status (captured by the MacArthur Scale of Subjective Social Status) is in many cases a stronger predictor of health outcomes than objective socioeconomic status (SES).PurposeThe study aims to test whether implicit beliefs about social class moderate the relationship between subjective social status and inflammation.MethodsWe measured implicit social class bias, subjective social status, SES, and baseline levels of interleukin-6 (IL-6), a marker of inflammation, in 209 healthy adults.ResultsImplicit social class bias significantly moderated the relationship between subjective social status and levels of IL-6, with a stronger implicit association between the concepts "lower class" and "bad" predicting greater levels of IL-6.ConclusionsImplicit social class bias moderates the relationship between subjective social status and health outcomes via regulation of levels of the inflammatory cytokine IL-6. High implicit social class bias, particularly when one perceives oneself as having low social standing, may increase vulnerability to inflammatory processes.

Background: Historical loss in American Indians (AIs) is believed to contribute to high incidence of mental health disorders, yet less is known about the associations between historical loss and physical health.Purpose: To investigate whether frequency of thought about historical loss predicts risk factors for chronic physical health conditions in an AI community.Methods: Using Community Based Participatory research (CBPR) and Ecological Momentary Assessment (EMA), we measured frequency of thoughts about historical loss in 100 AI adults residing on the Blackfeet reservation. Participants completed a 1-week monitoring period, during which ambulatory blood pressure and daily levels of psychological stress were measured. At the end of the week, we collected a dried blood spot sample for measurement of C-reactive protein (CRP).Results: In hierarchical linear regression models controlling for demographics and relevant covariates, greater frequency of thoughts about historical loss predicted higher average daily psychological stress (B = .55, t = 6.47, p < .001, ΔR2 = .30) and higher levels of CRP (B = .33, t = 3.93, p < .001, ΔR2 = .10). Using linear mixed modeling with relevant covariates, we found that greater thoughts about historical loss were associated with higher systolic ambulatory blood pressure (B = .32, 95% CI = .22-.42, t = 6.48, p < .001, ΔR2 = .25; Fig. 1c) and greater diastolic ambulatory blood pressure (B = .19, 95% CI = .11-.27, t = 4.73, p < .001, ΔR2 = .19).Conclusions: The data suggest that frequency of thought about historical loss may contribute to increased subclinical risk for cardiovascular disease in the Blackfeet community. [ABSTRACT FROM AUTHOR]

It is proposed that environmental exposures in early life influence immune programming. Specifically, socioeconomic disadvantage is thought to program an immune phenotype that is prone to inflammation and associated with increased risk for inflammatory disease later in life. Existing literature shows an inverse association of early childhood socioeconomic status (SES) with adult levels of systemic inflammation. Here, we extend that literature to examine whether early childhood SES also relates to the magnitude of inflammatory response to acute psychological stress in adulthood. Healthy volunteers (N = 110; 40–58 years; 59% female; 90% white) performed a laboratory stress protocol, with blood samples drawn at the end of a 30-min baseline, a 5-min speech task, and a 30-min recovery to assess interleukin (IL)-6 stress responses. An early childhood SES index was derived from reports of parental home and vehicle ownership, and number of bedrooms per child in the home across ages 1–2, 3–4, and 5–6. Regressions adjusted for current age, sex, race, and BMI showed that lower SES at age 1–2 was associated with larger IL-6 stress responses in adulthood (ΔR 2  = 0.05, β = −0.24, p  = .03). This association was independent of adult SES and task-evoked affective responses. No association was found between SES at ages 3–4 or 5–6 and IL-6 responses. These results provide initial evidence for a link between disadvantage in the first 2 years of life and heightened inflammatory response to stress in adulthood; this link may contribute to the increased disease risk that accompanies being raised in disadvantaged socioeconomic circumstances. [ABSTRACT FROM AUTHOR]

This research independently manipulated two potential attenuators of stereotype threat – reappraisal of anxiety and test framing – to explore their independent and combined effects. Female participants took a difficult math exam that was described as gender-biased or gender-fair and were told that anxious arousal could positively impact performance or were given no information regarding arousal. Levels of the cytokine Interleukin-6 (IL-6), an immune marker of inflammation, were measured in oral mucosal transudate (OMT) both before and after the exam. Our findings indicate that directing reappraisal of physiological arousal attenuated increases in IL-6 across test framing conditions, and was especially effective under stereotype threat (i.e., gender-biased test condition). Reappraisal also mapped onto better test performance in the threat condition. Together, these findings provide insight into the unique and interactive effects of two situational interventions meant to reduce stereotype threat, indexed here by both physiological and performance-based correlates of threat. [ABSTRACT FROM AUTHOR]