Psychological distress may contribute to chronic activation of acute-phase inflammation. The current study investigated how financial stressors influence psychosocial functioning and inflammation. This study examined a) the direct relations between financial stress and inflammation; b) whether the relationships between financial stress and inflammation are mediated in part by negative interpersonal events, psychological distress, and psychological well-being; and c) whether social standing in one's community moderates the relations between financial stress and psychological distress, psychological well-being, and markers of inflammation (interleukin-6 [IL-6] and C-reactive protein).
Stressful financial and interpersonal events over the previous year, perceived social status, indices of psychological well-being and distress, and levels of IL-6 and C-reactive protein were assessed in a community sample of 680 middle-aged adults (ages 40–65 years).
Structural equation modeling analyses revealed significant relations among financial stress, interpersonal stress, and psychological distress and well-being, and complex relationships between these variables and inflammatory markers. Psychological well-being mediated the association between financial stress and IL-6 ([mediation] ab = 0.012, standard error [SE] = 0.006, p = .048). Furthermore, individuals with higher perceived social standing within their communities exhibited a stronger relation between negative financial events and both interpersonal stressors (interaction B = 0.067, SE = 0.017, p < .001) and C-reactive protein (interaction B = 0.051, SE = 0.026, p = .050).
Financial stress demonstrates complex relations with inflammation, due partly to psychological well-being and social perceptions. Findings are discussed with regard to the social context of stress and physiological factors pertinent to stress adaptation and inflammation.
From the Department of Anesthesiology, Perioperative and Pain Medicine (Sturgeon), Stanford University, Palo Alto, California; Department of Psychology (Arewasikporn, Okun, Davis, Zautra), Arizona State University, Tempe, Arizona; and Department of Human Development (Ong), Cornell University, Ithaca, New York.
Address correspondence and reprint requests to John A. Sturgeon, PhD, Stanford Systems Neuroscience and Pain Laboratory, Department of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, 1070 Arastradero, Suite 200, MC 5596, Palo Alto, CA 94305. E-mail: email@example.com
Received for publication August 12, 2014; revision received September 16, 2015.