Stressful life events across the lifespan and inflammation: An integrative data analysis

Experiencing more stressful life events has been linked to higher levels of inflammation, but this association may depend on when in the lifespan the stressors occur. To address this knowledge gap, we tested two lifespan theories, the accumulation of risks and sensitive period models, by assessing the association between the total number of stressful events and their life stage occurrence on later-life C-reactive protein (CRP). We harmonized data across two cohort studies, maximizing variation in stressors reported across the lifespan. Participants (N_total = 7,952, 57.7% female, M_age = 69) from the Health and Retirement Study (HRS: n = 5,136, M_age = 70.6) and the English Longitudinal Study of Aging (ELSA: n = 2,816, M_age = 66.1) completed retrospective surveys of stressful life events and indicated what year(s) each event occurred and had blood drawn ∼4.5 years later. Stressful events were summed across the participants’ lifespans (age 0 to current age) and within childhood (0–17 years), young adulthood (18–39), midlife (40–59), and late adulthood (60+). In main effects models, more cumulative stressors (γ = .05, SE = .02, p = .012) and stressors in young adulthood (γ = .06, SE = .03, p = .037) were associated with higher levels of CRP. In models with all life stages together among adults age 65+ (n = 4,972), experiencing more stressors in midlife significantly predicted higher levels of CRP (γ = .08, SE = .04, p = .038). Our findings replicate prior evidence of an association between cumulative stressors and inflammation and extend this work by identifying stressors in young adulthood and midlife as potentially unique sensitive periods that predict higher levels of later-life inflammation.