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Reminiscing about positive memories buffers acute stress responses.

ABSTRACT: Recalling happy memories elicits positive feelings and enhances one's wellbeing, suggesting a potential adaptive function in using this strategy for coping with stress. In two studies, we explored whether recalling autobiographical memories that have a positive content - i.e., remembering the good times - can dampen the hypothalamic-pituitary-adrenal (HPA) axis stress response. Participants underwent an acute stressor or control task followed by autobiographical memory recollection (of only positive or neutral valence). Across both studies, recalling positive, but not neutral, memories resulted in a dampened cortisol rise and reduced negative affect. Further, individuals with greater self-reported resiliency showed enhanced mood, despite stress exposure. During positive reminiscence, we observed engagement of corticostriatal circuits previously implicated in reward-processing and emotion regulation, and stronger connectivity between ventrolateral and dorsolateral prefrontal cortex as a function of positivity. These findings highlight the restorative and protective function of self-generated positive emotions via memory recall in the face of stress.

SUBMITTER: Speer ME

PROVIDER: S-EPMC6719713 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature

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Reminiscing about positive memories buffers acute stress responses.

Speer Megan E ME Delgado Mauricio R MR

Nature human behaviour 20170424 5

Recalling happy memories elicits positive feelings and enhances one's wellbeing, suggesting a potential adaptive function in using this strategy for coping with stress. In two studies, we explored whether recalling autobiographical memories that have a positive content - i.e., remembering the good times - can dampen the hypothalamic-pituitary-adrenal (HPA) axis stress response. Participants underwent an acute stressor or control task followed by autobiographical memory recollection (of only posi ...[more]

PMID: 31482135

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Project description:BackgroundInvoluntary memories are a hallmark symptom of posttraumatic stress disorder (PTSD), but studies of the neural basis of involuntary memory retrieval in posttraumatic stress disorder (PTSD) are sparse. The study of the neural correlates of involuntary memories of stressful events in PTSD focuses on the voluntary retrieval of memories that are sometimes recalled as intrusive involuntary memories, not on involuntary retrieval while being scanned. Involuntary memory retrieval in controls has been shown to elicit activity in the parahippocampal gyrus, precuneus, inferior parietal cortex, and posterior midline regions. However, it is unknown whether involuntary memories are supported by the same mechanisms in PTSD. Because previous work has shown that both behavioral and neural responsivity is slowed in PTSD, we examined the spatiotemporal dynamics of the neural activity underlying negative and neutral involuntary memory retrieval.MethodsTwenty-one individuals with PTSD and 21 non-PTSD, trauma-exposed controls performed an involuntary memory task, while undergoing a functional magnetic resonance imaging scan. Environmental sounds served as cues for well-associated pictures of negative and neutral scenes. We used a finite impulse response model to analyze temporal differences between groups in neural responses.ResultsCompared with controls, participants with PTSD reported more involuntary memories, which were more emotional and more vivid, but which activated a similar network of regions. However, compared to controls, individuals with PTSD showed delayed neural responsivity in this network and increased vmPFC/ACC activity for negative > neutral stimuli.ConclusionsThe similarity between PTSD and controls in neural substrates underlying involuntary memories suggests that, unlike voluntary memories, involuntary memories elicit similar activity in regions critical for memory retrieval. Further, the delayed neural responsivity for involuntary memories in PTSD suggests that factors affecting cognition in PTSD, like increased fatigue, or avoidance behaviors could do so by delaying activity in regions necessary for cognitive processing. Finally, compared to neutral memories, negative involuntary memories elicit hyperactivity in the vmPFC, whereas the vmPFC is typically shown to be hypoactive in PTSD during voluntary memory retrieval. These patterns suggest that considering both the temporal dynamics of cognitive processes as well as involuntary cognitive processes would improve existing neurobiological models of PTSD.

Project description:BackgroundSleep disturbances and insufficient sleep are highly prevalent. Both clinical sleep disorders and multiple forms of experimental sleep loss predict heightened inflammation. As such, it is necessary to investigate potential protective factors. Given that trait positive affect (PA) is associated with reduced inflammation, and buffers the proinflammatory effects of stress, it is possible that high trait positive affect might protect individuals from an inflammatory response to sleep disruption. The present study tested this hypothesis in an experimental sleep disruption paradigm with assessment of cellular inflammation.MethodsData were drawn from good sleeping adults (n = 79) who participated in a randomized, within-subjects crossover experiment comparing the effects of two nights of sleep disruption versus two nights of uninterrupted sleep. Stimulated monocytic production of intracellular proinflammatory cytokines tumor necrosis factor (TNF) and interleukin-6 (IL-6) were assayed using flow cytometric methods and indexed as the percentage of monocytes expressing TNF, IL-6, or co-expressing both. Hypotheses were evaluated using linear mixed effects models.ResultsControlling for negative affect, body mass index, age, and sex, PA significantly moderated the associations between sleep condition and stimulated monocyte production of IL-6 (b = -1.03, t = -2.02, p = .048) and its co-expression with TNF (b = -0.93, t = -2.00, p = .049), such that inflammatory responses were blunted among those high in PA with increases principally among those low in PA. The effect on TNF was similar in terms of effect size, but marginally significant.ConclusionsActivation of cellular inflammation in response to sleep disruption is buffered by PA independent of negative affect. Interventions that promote PA might protect persons from the inflammatory activation following sleep loss, with the potential to mitigate the adverse health consequences of sleep disturbance.

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Reminiscing about positive memories buffers acute stress responses.

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Reminiscing about positive memories buffers acute stress responses.

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