Daily life stress reactivity in remitted versus non-remitted depressed individuals

Winkel, M. van; Nicolson, Nancy A.; Wichers, Marieke; Viechtbauer, Wolfgang; Myin-Germeys, Inez; Peeters, Frenk

doi:10.1016/j.eurpsy.2015.02.011

Cited by 66 publications

(63 citation statements)

References 46 publications

(74 reference statements)

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“…No negative effects were observed of the TSST, as would be expected [30]. However, it should be noted that in previous studies, mood was measured directly after the TSST, while in this study mood was only first measured 60 min postintervention.…”

Section: Discussionmentioning

confidence: 63%

Differential Effects of Inflammatory and Psychosocial Stress on Mood, Hypothalamic-Pituitary-Adrenal Axis, and Inflammation in Remitted Depression

et al. 2016

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Background/Aims: Major depressive disorder (MDD) is highly recurrent. This may be due to increased stress sensitivity after remission. Both inflammatory and psychosocial stressors are implicated in the pathogenesis of MDD, but the additive or differential effect is unclear. Methods: We conducted a single-blind placebo-controlled study to investigate the effects of inflammatory stress (i.e., typhoid vaccination), psychosocial stress (i.e., Trier Social Stress Test [TSST]), or a combination of both in women (25-45 years old) with (partially) remitted recurrent MDD (n = 21) and healthy female controls (n = 18). We evaluated the effect on mood measured by the Profile of Mood States, markers of the hypothalamic-pituitary-adrenal (HPA) axis activity, and inflammatory system activation. The study was performed during 2 testing days, separated by a washout of 7-14 days. In a crossover design, subjects received one of the interventions on one day and placebo on the other. Results: A lowering of mood was seen in patients (β [95% CI] = -4.79 [-6.82 to -2.75], p < 0.001) only after vaccination, but not after the TSST or the combination; this effect was not observed in controls. Controls experienced a significantly different response on adrenocorticotropic hormone (ACTH) after vaccination, with a general rise in ACTH not observed in patients. In both groups, the TSST activated the HPA axis and suppressed the inflammatory parameters. Conclusions: There is a differential effect of inflammatory and psychosocial stress on mood and HPA axis activation in patients with remitted recurrent MDD. This may be an interesting treatment target in MDD.

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Section: Discussionmentioning

confidence: 63%

Differential Effects of Inflammatory and Psychosocial Stress on Mood, Hypothalamic-Pituitary-Adrenal Axis, and Inflammation in Remitted Depression

et al. 2016

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“…Heightened reactivity to everyday stressors, in turn, predicts the onset of future internalizing symptoms and episodes, characterizes patients with acute anxiety disorders and depression, and remits with pharmacological therapy (Farmer & Kashdan, 2015; Tan et al, 2012; van Winkel et al, 2015; Wichers et al, 2009). …”

Section: Trait-state Links Inferred From Self-report and Behaviormentioning

confidence: 99%

Dispositional negativity: An integrative psychological and neurobiological perspective.

Shackman¹,

Tromp²,

Stockbridge³

et al. 2016

Psychological Bulletin

207

208

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Dispositional negativity—the propensity to experience and express more frequent, intense, or enduring negative affect—is a fundamental dimension of childhood temperament and adult personality. Elevated levels of dispositional negativity can have profound consequences for health, wealth, and happiness, drawing the attention of clinicians, researchers, and policy makers. Here, we highlight recent advances in our understanding of the psychological and neurobiological processes linking stable individual differences in dispositional negativity to momentary emotional states. Self-report data suggest that three key pathways—increased stressor reactivity, tonic increases in negative affect, and increased stressor exposure—explain most of the heightened negative affect that characterizes individuals with a more negative disposition. Of these three pathways, tonically elevated, indiscriminate negative affect appears to be most central to daily life and most relevant to the development of psychopathology. New behavioral and biological data provide insights into the neural systems underlying these three pathways and motivate the hypothesis that seemingly ‘tonic’ increases in negative affect may actually reflect increased reactivity to stressors that are remote, uncertain, or diffuse. Research focused on humans, monkeys, and rodents suggests that this indiscriminate negative affect reflects trait-like variation in the activity and connectivity of several key brain regions, including the central extended amygdala and parts of the prefrontal cortex. Collectively, these observations provide an integrative psychobiological framework for understanding the dynamic cascade of processes that bind emotional traits to emotional states and, ultimately, to emotional disorders and other kinds of adverse outcomes.

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“…Additionally, patients suffering a depressive episode or in remission from depression exhibit increased sensitivity to social stressors encountered in daily life, indicating the robust nature of this stressor (van Winkel et al., 2015). Social stress and depression can affect anyone regardless of age, gender, ethnicity, or socio-economic background; however only a portion of the population is susceptible.…”

Section: Social Stress and Coping In Humansmentioning

confidence: 99%

Neuroinflammation at the interface of depression and cardiovascular disease: Evidence from rodent models of social stress

Finnell

Wood

2016

Neurobiology of Stress

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A large body of evidence has emerged linking stressful experiences, particularly from one's social environment, with psychiatric disorders. However, vast individual differences emerge in susceptibility to developing stress-related pathology which may be due to distinct differences in the inflammatory response to social stress. Furthermore, depression is an independent risk factor for cardiovascular disease, another inflammatory-related disease, and results in increased mortality in depressed patients. This review is focused on discussing evidence for stress exposure resulting in persistent or sensitized inflammation in one individual while this response is lacking in others. Particular focus will be directed towards reviewing the literature underlying the impact that neuroinflammation has on neurotransmitters and neuropeptides that could be involved in the pathogenesis of comorbid depression and cardiovascular disease. Finally, the theme throughout the review will be to explore the notion that stress-induced inflammation is a key player in the high rate of comorbidity between psychosocial disorders and cardiovascular disease.

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Daily life stress reactivity in remitted versus non-remitted depressed individuals

Abstract: Greater stress reactivity to event and activity stress appears to be state-dependent. The heightened social stress reactivity in remitted patients suggests that sensitivity to social stress may reflect an underlying vulnerability in MDD.

Cited by 66 publications

References 46 publications

Differential Effects of Inflammatory and Psychosocial Stress on Mood, Hypothalamic-Pituitary-Adrenal Axis, and Inflammation in Remitted Depression

Differential Effects of Inflammatory and Psychosocial Stress on Mood, Hypothalamic-Pituitary-Adrenal Axis, and Inflammation in Remitted Depression

Dispositional negativity: An integrative psychological and neurobiological perspective.

Neuroinflammation at the interface of depression and cardiovascular disease: Evidence from rodent models of social stress

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