Abstract
Recent work suggests effective emotion regulation may protect against risk of developing coronary heart disease (CHD), but the mechanisms remain unknown. Strategies for regulating emotions vary in how effectively they mitigate potentially toxic effects of stressful life experiences, and therefore may be differentially associated with CHD risk. In this study, we examined the emotion regulation strategies of reappraisal and suppression in relation to inflammation, a biological state associated with both stress and CHD. We hypothesized that suppression would be associated with elevated inflammation and reappraisal would be associated with lower levels of inflammation. We studied adult offspring (n = 379; mean age = 42.2 years) of Collaborative Perinatal Project participants, a national cohort of pregnant women enrolled in 1959-1966. Validated measures of two emotion regulation strategies were examined: reappraisal and suppression. Inflammation was measured as plasma C-reactive protein (CRP) levels. We fit multiple linear regression models predicting CRP while controlling for demographic, socioeconomic, and health factors, including depressive symptoms, measured across the life course. A 1 standard deviation increase in reappraisal was associated with significantly lower CRP (b = -0.18, SE = 0.06, p < .01) controlling for demographics. This relation was somewhat attenuated in life course models, with adulthood body mass index partially explaining the association. A 1 standard deviation increase in suppression was associated with significantly higher CRP (b = 0.21, SE = 0.05, p < .001), and this association was not substantively attenuated with further covariate adjustment. Adaptive emotion regulation was associated with lower levels of inflammation and maladaptive emotion regulation was associated with higher levels of inflammation. If these associations are confirmed by prospective and experimental studies, such evidence may provide insight into novel targets for interventions to promote health and reduce cardiovascular risk.
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