Stress and depression: old questions, new approaches

Abstract

After decades in which diatheses dominated research on the diathesis-stress models of depression, increasing attention to stress and stress-depression mechanisms is in the forefront of efforts to understand depression and treat it effectively. Supplementing research on known risk factors and moderators (such as demographic, cognitive, relational, family, and personality characteristics) of the stress-depression association, much work now focuses on experiences of early life stress, acute stressors, and chronic stress and their developmental features and neurobiological mechanisms relevant to depression. The review briefly highlights the current status of risk factors, HPA axis, neural, and genetic approaches, noting conceptual and methodological challenges.

Acute stress impairs frontocingulate activation during error monitoring in remitted depression

“…Mechanisms underlying risk for recurrence in remitted (rMDD) individuals are not fully understood, but may involve changes in cognitive control that persist beyond the resolution of outward signs and symptoms. Furthermore, independent lines of evidence show stress exposure both predicts depression recurrence (Hammen, 2015) and impairs prefrontal function (Arnsten, 2015). Accordingly, stress may trigger recurrence by uncovering or exacerbating cognitive control deficits in rMDD individuals, as cognitive control depends on prefrontal function (Ridderinkhof et al, 2004).…”

“…Furthermore, given the wealth of evidence linking stress to prefrontal dysfunction (Arnsten, 2015) and depression onset and maintennce (Hammen, 2015), it would be valuable to know whether depression history increases risk for error monitoring deficits following stress exposure. Although no studies to date have addressed this question, individuals with rMDD may experience greater stress-induced impairments in error monitoring for two reasons: 1) if individuals with rMDD are more sensitive to stress, the increased prefrontal resources required to regulate the stress response may deplete resources available for more cognitive aspects of performance monitoring, and 2) frontocingulate abnormalities that persist beyond remission may reduce the overall capacity for concurrent stress regulation and error monitoring.…”

Leisure behavior and sense of coherence in the context of depression

“…Research has established a strong link between stress and depression. It has been demonstrated that stress is relevant to depression, as stress is associated with onset as well as relapses and recurrences of depression (Hammen, ; Monroe, Slavich, & Georgiades, ). Stress, at the same time, is associated with depressive symptoms in the present, as individuals who perceive more stress experience elevated depressive symptoms (Monroe, Harkness, Simons, & Thase, ; Muscatell, Slavich, Monroe, & Gotlib, ).…”

“…While stress can be considered as both objective external factors and internal perceptual factors, Lazarus and Folkman () offered a transactional approach in which stress results from personal appraisal of the environment in which environmental demands are perceived as exceeding or taxing one's resources to respond. Individuals with depression are particularly vulnerable to stress, due to a weakened stress‐resistance capacity (Carstens & Spangenberg, ; Skärsäter et al, ) which can result in exacerbated depressive symptoms (Hammen, ; Pittenger & Duman, ). Therefore, identification of resources among people with depression that may be mobilized to resist the ill effects of stress provides targets for therapeutic intervention.…”

Editorial overview: The assessment, etiology, and treatment of unipolar depression

“…Given the central role that life stress plays in depression, Hammen (2015) provides an in-depth review of this research literature. Specifically, she reviews cutting edge research on how early life stress, acute stressors, and chronic stress each contribute to depression, both alone and in conjunction with known risk factors and moderators, such as individual differences in HPA axis, neural and genetic mechanisms.…”