Hostinar et al., 2015. Additive contributions of childhood adversity and recent stressors to inflammation at midlife: Findings from the MIDUS study.

Hostinar, C. E., Lachman, M. E., Mroczek, D. K., Seeman, T. E., & Miller, G. E. (2015). Additive contributions of childhood adversity and recent stressors to inflammation at midlife: Findings from the MIDUS study. Developmental psychology, 51(11), 1630.

Year: 
2015
Status: 
complete
Abstract: 

We examined the joint contributions of self-reported adverse childhood experiences (ACEs) and recent life events (RLEs) to inflammation at midlife, by testing 3 competing theoretical models: stress generation, stress accumulation, and early life stress sensitization. We aimed to identify potential mediators between adversity and inflammation. Participants were 1,180 middle-aged and older adults from the Midlife in the United States (MIDUS) Biomarker Project (M age = 57.3 years, SD = 11.5; 56% female). A composite measure of inflammation was derived from 5 biomarkers: serum levels of C-reactive protein, interleukin-6, fibrinogen, E-selectin, and ICAM-1. Participants provided self-report data regarding ACEs, RLEs, current lifestyle indices (cigarette smoking, alcohol consumption, physical exercise, waist circumference), current depressive symptoms, and demographic/biomedical characteristics. We also used indices of hypothalamic–pituitary–adrenocortical outflow (12-hr urinary cortisol) and sympathetic nervous system output (12-hr urinary norepinephrine and epinephrine). Analyses indicated that ACEs and RLEs were independently associated with higher levels of inflammation, controlling for each other’s effects. Their interaction was not significant. The results were consistent with the hypothesis that associations between ACEs and inflammation were mediated through higher urinary norepinephrine output, greater waist circumference, smoking, and lower levels of exercise, whereas higher waist circumference and more smoking partially mediated the association between RLEs and inflammation. In support of the stress accumulation model, ACEs and RLEs had unique and additive contributions to inflammation at midlife, with no evidence of synergistic effects. Results also suggested that norepinephrine output and lifestyle indices may help explain how prior stressors foster inflammation at midlife. (PsycINFO Database Record (c) 2016 APA, all rights reserved)

 

Friedman et al., 2015. Inflammation Partially Mediates the Association of Multimorbidity and Functional Limitations in a National Sample of Middle-Aged and Older Adults: The MIDUS Study

Friedman, E. M., Christ, S. L., & Mroczek, D. K. (2015). Inflammation partially mediates the association of multimorbidity and functional limitations in a national sample of middle-aged and older adults: The MIDUS Study. Journal of aging and health, 27(5), 843-863.DOI: 10.1177/0898264315569453

Year: 
2015
Status: 
complete
Abstract: 

Objective: Older adults are increasingly likely to have two or more chronic medical conditions (multimorbidity) and are consequently at greater risk of disability. Here we examine the role of inflammation in mediating the relationship between multimorbidity and disability. 

Method: Data are from the Survey of Mid-Life in the United States (MIDUS), a national sample of middle-aged and older adults. Structural equation models were used to assess direct relationships between multimorbidity and activities of daily living as well as indirect associations with a latent variable for inflammation (indicated by circulating levels of interleukin-6, C-reactive protein, and fibrinogen) as a mediator. 

Results: After adjustment for potential confounds, multimorbidity was positively associated with inflammation (p < .001) and functional limitations (p < .001), and inflammation partially mediated the link between multimorbidity and functional limitations (p < .01). 

Discussion: Inflammation may be an important biological mechanism through which chronic medical conditions are linked to disability in later life.