Laboratory stress paradigms provide standardized methods for examining stress reactivity. In fact, inflammation plays a key role in depression’s pathogenesis for a subset of depressed individuals ( Kiecolt-Glaser et al., 2015). Although the immune system’s acute inflammatory response to infection or trauma is beneficial, chronic inflammation characterizes multiple systemic diseases and disorders including cardiovascular disease, metabolic syndrome, diabetes, asthma, arthritis, psoriasis, and chronic pain among others, and each of these also carries an increased risk for depression ( Kiecolt-Glaser, Derry, & Fagundes, 2015). Beyond physiological responding, HRV is related to cognitive, emotional, and social processes, e.g., individuals with lower HRV are less able to respond flexibly during stress ( Appelhans & Luecken, 2006), and lower HRV can promote inflammation ( Williams et al., 2019). The PNS opposes the “fight-or-flight” response of the sympathetic nervous system (SNS), and when PNS activity is low (reflected by lower heart rate variability HRV), the body’s stress response remains uncontested, facilitating autonomic arousal (sympathetic dominance). For example, parasympathetic nervous system (PNS) functioning-the body’s rest and digest system-did not vary between depressed and nondepressed individuals during resting states, but differences emerged when confronting a stressor ( Hu, Lamers, de Geus, & Penninx, 2016). Reactivity to stressors yields insights into health-related risks that cannot be gleaned from resting measurements. Although many people habituate to a repeated stressor, unpredictable and uncontrollable stressors more reliably evoke cardiovascular, neuroendocrine, and inflammatory responses. In the context of a recurring stressor (e.g., parents managing their young child’s tantrums), a failure to habituate, or recognize the relative safety of this repeating scenario, provokes an unnecessary physiological response. In contrast, an adaptive stress response is flexible and short-lived. Prestressor worry and post-stressor rumination prolong the stressor’s effects worry provokes an anticipatory response, and rumination hinders a return to baseline. An exaggerated response needlessly taxes the body, preparing it for action that may be inappropriate for instance, many modern stressors, like receiving critical feedback from a supervisor, are not life-threatening and do not require a “fight-or-flight” response, yet the stress response mobilizes energy reserves (e.g., glucose) for the exaggerated response. Although we focus on amplified and long-lasting reactivity, low responsiveness can also be problematic ( Turner et al., 2020).Ī stress response is adaptive when its magnitude aligns with the stressor’s threat and the body can return to a resting state soon after the threat ends. The body’s acute responses to daily stressors can differ widely among individuals experiencing the same stressor, and these physiological responses may not align with stress appraisals ( Campbell & Ehlert, 2012 Turner et al., 2020).The hormonal, cardiovascular, and inflammatory responses to stress are biologically adaptive, readying the body for action and possible injury, but a heightened or prolonged response, especially in the context of modern stressors that do not require fighting or fleeing, promotes biological wear and tear that can shape health trajectories ( McEwen, 1998). Stress Reactivity: What Pushes Us Higher, Faster, and Longer – and Why It Mattersīrief everyday stressors are inherent in life, but their health consequences vary based on individual differences in physiological stress reactivity. Interventions that may dampen physiological stress reactivity include yoga, meditation, health behaviors (diet, exercise, and sleep), and cognitive behavioral therapy. Heightened and prolonged stress reactivity can provide a gateway to the physiological dysregulation that underlies depression and chronic disease, which themselves alter stress reactivity – a vicious cycle. We discuss depression, rumination, early life adversity, and social evaluation as individual level factors, and interpersonal stress processes and relationship quality as dyadic level factors that may influence physiological stress responses. This review highlights individual and dyadic factors that may heighten and prolong stress reactivity, and their implications for health. Acute responses to daily stressors can vary widely among individuals experiencing the same stressor, and these physiological responses may not align with stress appraisals. Brief everyday stressors can provoke cardiovascular, hormonal, and immune changes, with considerable variation in the magnitude and duration of these responses.
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