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 < .001), IL-6 (d = 0.35, p < .001), IL-10 (d = 0.69, p < .001), and tumor necrosis factor(TNF)-α (d = 0.28, p < .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 120 min following stress, with the largest effect at 90min post-stress (d = 0.70, p < .001). IL-1β increased from baseline to 20–30, 40–50, and 60–70 min following stress, with the largest effect between 40–50 min post-stress (d = .73, p = .02). For TNF-α, there was a significant increase from baseline to 31–50 min post stress (d = 0.44, p = .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 20–120 min post-stress (d = 1.09, p < .001), and in IL-4 and interferon-γ when measured 0–10 min post stressor (d = −0.42, p < .001 and d = 0.47, p < .001). These results extend findings from a prior meta-analysis (Steptoe, Hamer, & Chida, 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.

Despite the strong evidence linking psychological stress to disease risk, health researchers often fail to include psychological stress in models of health. One reason for this is the incorrect perception that the construct of psychological stress is too vague and broad to accurately measure. This article describes best practices in stress measurement, detailing which dimensions of stressor exposures and stress responses to capture, and how. We describe when to use psychological versus physiological indicators of stress. It is crucial that researchers across disciplines utilize the latest methods for measuring and describing psychological stress in order to build a cumulative science.

There are distinct racial disparities in cardiovascular disease (CVD) risk, with Black individuals at much greater risk than White individuals. Although many factors contribute to these disparities, recent attention has focused on the role of discrimination as a stress-related factor that contributes to racial disparities in CVD. As such, it is important to understand the mechanisms by which discrimination might affect CVD. Recent studies have examined these mechanisms by focusing on neurobiological mediators of CVD risk. Given this increase in studies, a systematic review of perceived discrimination and neurobiological mediators of CVD risk is warranted. Our review uses a multisystem approach to review studies on the relationship between perceived discrimination and (1) cardiovascular responses to stress, (2) hypothalamic-pituitary-adrenocortical axis function, and (3) the immune system, as well as (4) the brain systems thought to regulate these parameters of peripheral physiology. In addition to summarizing existing evidence, our review integrates these findings into a conceptual model describing multidirectional pathways linking perceived discrimination with a CVD risk.

Cancer-related fatigue is a common and often long lasting symptom for many breast cancer survivors. Fatigued survivors show evidence of elevated inflammation, but the physiological mechanisms driving inflammatory activity have not been determined. Alterations in the autonomic nervous system, and particularly parasympathetic nervous system activity, are a plausible, yet understudied contributor to cancer-related fatigue. The goal of this study was to replicate one previous study showing an association between lower parasympathetic activity and higher fatigue in breast cancer survivors (Fagundes et al., 2011), and to examine whether inflammation mediates this association. Study participants were drawn from two samples and included 84 women originally diagnosed with early-stage breast cancer prior to age 50. Participants completed questionnaires, provided blood samples for determination of interleukin (IL)-6 and C-reactive protein (CRP), and underwent electrocardiography (ECG) assessment for evaluation of resting heart rate variability (HRV), a measure of parasympathetic activity. Results showed that lower HRV was associated with higher fatigue (p < .05), as predicted. In bivariate analyses, HRV was also correlated with circulating concentrations of IL-6 and CRP. However, path analyses did not support inflammation as a mediator of the association between HRV and fatigue; instead, associations among these variables appeared to be driven by age and BMI. These findings identify HRV as a potential contributor to cancer-related fatigue, but suggest that inflammation does not mediate this association in younger, healthy breast cancer survivors who are several years post-treatment. The autonomic nervous system merits additional attention in research on the etiology of cancer-related fatigue.

No abstract