Rebecca G Reed1, Iris B Mauss2, Nilam Ram3, Suzanne C Segerstrom4. 1. Department of Psychology, University of Pittsburgh, 210 S. Bouquet St., Pittsburgh, PA, 15260, USA. rebecca.reed@pitt.edu. 2. Department of Psychology, University of California, Berkeley, USA. 3. Departments of Communication and Psychology, Stanford University, Stanford, USA. 4. Department of Psychology, University of Kentucky, Lexington, USA.
Abstract
BACKGROUND: The current study (1) examined links between daily stressors and inflammation and (2) tested whether negative emotion dynamics (emotional variability) is one pathway through which stressors are linked to inflammation. METHOD: A cross-sectional sample of 986 adults (aged 35-86 years, 57% female) from MIDUS reported daily stressor frequency and severity and negative emotions on 8 consecutive nights. Negative emotion variability (intraindividual standard deviation), controlling for overall mean level (intraindividual mean), was the focus of the current study. Interleukin-6 (IL-6) and C-reactive protein (CRP) were assayed from blood drawn at a clinic visit. Regression models adjusted for demographics, health factors, and the time between assessments. RESULTS: More severe daily stressors were associated with higher CRP, but this effect was accounted for by covariates. More frequent daily stressors were associated with lower IL-6 and CRP. In follow-up analyses, significant interactions between stressor severity and frequency suggested that participants with lower stressor severity and higher stressor frequency had the lowest levels of IL-6 and CRP, whereas those with higher stressor severity had the highest levels of IL-6 and CRP, regardless of frequency. Daily stressor frequency and severity were positively associated with negative emotion variability, but variability was not linearly associated with inflammation and did not operate as a mediator. CONCLUSION: Among midlife and older adults, daily stressor frequency and severity may interact and synergistically associate with inflammatory markers, potentially due to these adults being advantaged in other ways related to lower inflammation, or in a pattern aligning with hormetic stress, where frequent but manageable stressors may yield physiological benefits, or both. Negative emotion variability does not operate as a mediator. Additional work is needed to reliably measure and test other emotion dynamic metrics that may contribute to inflammation.
BACKGROUND: The current study (1) examined links between daily stressors and inflammation and (2) tested whether negative emotion dynamics (emotional variability) is one pathway through which stressors are linked to inflammation. METHOD: A cross-sectional sample of 986 adults (aged 35-86 years, 57% female) from MIDUS reported daily stressor frequency and severity and negative emotions on 8 consecutive nights. Negative emotion variability (intraindividual standard deviation), controlling for overall mean level (intraindividual mean), was the focus of the current study. Interleukin-6 (IL-6) and C-reactive protein (CRP) were assayed from blood drawn at a clinic visit. Regression models adjusted for demographics, health factors, and the time between assessments. RESULTS: More severe daily stressors were associated with higher CRP, but this effect was accounted for by covariates. More frequent daily stressors were associated with lower IL-6 and CRP. In follow-up analyses, significant interactions between stressor severity and frequency suggested that participants with lower stressor severity and higher stressor frequency had the lowest levels of IL-6 and CRP, whereas those with higher stressor severity had the highest levels of IL-6 and CRP, regardless of frequency. Daily stressor frequency and severity were positively associated with negative emotion variability, but variability was not linearly associated with inflammation and did not operate as a mediator. CONCLUSION: Among midlife and older adults, daily stressor frequency and severity may interact and synergistically associate with inflammatory markers, potentially due to these adults being advantaged in other ways related to lower inflammation, or in a pattern aligning with hormetic stress, where frequent but manageable stressors may yield physiological benefits, or both. Negative emotion variability does not operate as a mediator. Additional work is needed to reliably measure and test other emotion dynamic metrics that may contribute to inflammation.
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