Stress and Disease: A Structural and Functional Analysis

Social and Personality Psychology Compass 7/4 (2013): 217–227, 10.1111/spc3.12020 Stress and Disease: A Structural and Functional Analysis Joshua Smyth*, Matthew Zawadzki, and William Gerin Pennsylvania State University Abstract Chronic stress, a validated health risk factor, remains an ambiguous construct in spite of years of research. We propose that chronic stress is best understood as a series of acute stress responses, and that these responses become maladaptive when they occur frequently or are of long duration. We focus on the factors that contribute to chronic stress: whether the presence of a stressor, real or imagined, is long-lived and ⁄ or frequent (repeated activation), the degree to which the stressor is perceived as a threat even when no longer present (low or slow adaptation), and the extent to which the duration of responding is prolonged (delayed or failure to return to homeostasis). Importantly, we examine how perseverative cognitions (such as rumination and worry) contribute to chronic stress by creating and sustaining acute stress responses, largely via influencing activation, adaptation, and return to homeostasis. Finally, we discuss the implications of our stress model: that interventions can be ideographically tailored to address how an individual is experiencing chronic stress; that researchers may be better able to identify specific characteristics of chronic stress that relate most strongly to poor health; and that moderators of chronic stress may function through these contributing factors rather than via general effects on the system. Introduction Everyone ‘‘knows’’ that stress is bad for you – we are told that it can make you ill and even kill you. Research generally supports this view; stress is related to the risk of cardio- vascular disease, HIV ⁄ AIDS, and major depression, with emerging evidence linking stress to upper respiratory tract infections, asthma, herpes viral infections, autoimmune diseases, and wound healing (e.g. Cohen, Janicki-Deverts, & Miller, 2007). Additionally, the liter- ature describing plausible biological pathways whereby chronic stress may influence dis- ease onset and ⁄ or progression is rapidly growing (see Miller, Chen, & Cole, 2009; for review). Recent reviews have concluded that stress is related to complex alterations in both endocrine (e.g. Miller, Chen, & Zhou, 2007) and immune processes (e.g. Byrne- Davis & Vedhara, 2008; Segerstrom, 2010), and highlighted large individual differences in response to stress. Some work also suggests that stress may impair normal genetic pro- cesses, notably DNA expression and repair (e.g. Flint, Baum, Chambers, & Jenkins, 2007; Kiecolt-Glaser, Stephens, Lipetz, Speicher, & Glaser, 1985). The Scope of This Paper In spite of the ubiquity of stress as a construct, and the tremendous amount of research on stress in behavioral medicine and health psychology, it remains a challenge to clearly label, model, and understand. Providing comprehensive reviews on the extensive comple- ment of stress theories is beyond the scope of this paper; where appropriate, we direct the reader to source material. The overarching purpose of this paper is to synthesize the major extant perspectives so as to provide a simple schematic for helping to understand a 2013 Blackwell Publishing Ltd