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Rumination about the past and worries about the future (perseverative cognition) are extremely common, although pervasive and distressing, dysfunctional cognitive processes. Perseverative cognition is not only implicated in psychological health, contributing to mood worsening and psychopathology but, due to its ability to elicit prolonged physiological activity, is also considered to play a role in somatic health. Although there is emerging evidence that such negative and persistent thoughts have consequences on the body, this association has not yet been quantified. The aim of this study was to meta-analyze available studies on the physiological concomitants of perseverative cognition in healthy subjects. Separate meta-analyses were performed on each examined physiological parameter. Sixty studies were eligible for the analyses. Associations emerged between perseverative cognition and higher systolic blood pressure (SBP) (g = .45) and diastolic blood pressure (DBP) (g = .51) in experimental studies, and higher heart rate (HR) (g = .28 and g = .20) and cortisol (g = .36 and g = .32), and lower heart rate variability (HRV) (g = .15 and g = .27) in experimental and correlational studies, respectively. Significant moderators were sex, ethnicity, type of induction used to elicit perseverative cognition, assessment of state versus trait perseverative cognition, focus on worry or rumination, duration of physiological assessment, and quality of the studies. With the exception of blood pressure, results were not influenced by publication bias. Results show that perseverative cognition affects cardiovascular, autonomic, and endocrine nervous system activity, suggesting a pathogenic pathway to long-term disease outcomes and clarifying the still unexplained relationship between chronic stress and health vulnerability., ((c) 2016 APA, all rights reserved).)

Objectives: This longitudinal study examined the associations between work stressors, perseverative cognition and subjective and objective sleep quality. We hypothesized work stressors to be associated with (i) poor nocturnal sleep quality and (ii) higher levels of perseverative cognition during a free evening. We further hypothesized (iii) perseverative cognition to be associated with poor nocturnal sleep quality and (iv) the association between work stressors and sleep quality to be mediated by perseverative cognition., Methods: The participants were 24 pilots working for the Dutch Helicopter Emergency Medical Service (HEMS). They completed six questionnaires: at the end of three consecutive day shifts and each morning following the shifts. The questionnaires addressed work stressors (workload, distressing shifts and work-related conflicts), subjective sleep quality and perseverative cognition. Participants wore actigraphs to assess sleep onset latency, total sleep time and number of awakenings., Results: Correlation analysis revealed that (i) distressing shifts were related to delayed sleep onset (r=0.50, p=0.026) and that workload was related to impaired sleep quality (e.g., subjective sleep quality: r=-0.42, p=0.044). Moreover, (ii) distressing shifts were positively related to perseverative cognition (r=0.62, p=0.002), (iii) perseverative cognition delayed sleep onset (r=0.74, p<0.001) and (iv) mediated the association between distressing shifts and sleep onset latency., Conclusions: Perseverative cognition may be an explanatory mechanism in the association between work stressors and poor sleep.

Prolonged physiological activity is believed to be a key factor mediating between stress and later disease outcomes. Few studies, however, have investigated the crucial psychological factors that cause prolonged activity. This article proposes that conscious as well as unconscious perseverative cognition are the critical factors. Perseverative cognition indicates repetitive or sustained activation of cognitive representations of past stressful events or feared events in the future. In daily life, most prolonged physiological activity is not due to stressful events but to perseverative cognition about them. We and others have already found evidence that conscious perseverative cognition, i.e., worry, has physiological effects, in both laboratory and real life settings, and that perseverative cognition mediates prolonged responses to stressful events. Yet, there are convincing reasons to expect that unconscious perseverative cognition has an even larger role in stress-related prolonged activity. Firstly, since the greater part of cognitive processing operates without awareness, a considerable part of perseverative cognition is likely to be unconscious too. People may not be aware of most of their stress-related cognitive processes. Secondly, our recent studies have shown that increased activity of the autonomic nervous system continues after conscious perseverative cognition has stopped: It goes on for several hours and even during sleep. This and several other findings suggest that a considerable part of increased physiological activity may be due to unconscious perseverative cognition. The article closes with suggesting methods to test unconscious perseverative cognition and ways to change it, and concludes with stating that the notion of unconscious perseverative cognition potentially opens an entirely new area within stress research., (Copyright © 2010 Elsevier Inc. All rights reserved.)

In daily life, not stressful events themselves but their sustained cognitive representation is likely to cause prolonged physiological activity, which is believed to lead to a pathogenic state and finally somatic disease. The typically human ability to make cognitive representations of past stressful events (rumination) or feared events in the future (worry) is called perseverative cognition (PC). PC is associated with increased activity in various bodily systems, and there is emerging evidence that it mediates the prolonged effects of stressors on physiology and on disease. Yet, there are strong reasons to believe that people may not be aware of the greater part of their stress-related cognitive processes, while several studies suggest that these processes may still cause increased physiological activity, during sleep as well as during waking. This may imply that unconscious PC is an even more important source of prolonged stress-related activity than conscious PC. Thus, 'unconscious stress' research has the potential to become a new important area and may yield new important markers of chronic stress.

Slow cardiovascular (CV) recovery after stress is a predictor of adverse CV outcomes. Perseverative cognition (PC) about stress has been hypothesized to co-determine slow recovery. In the present study, it was investigated whether two types of trait PC, i.e. trait worry and trait rumination, predicted delayed cardiac recovery after a cognitive stressor. Furthermore, it was examined whether explicit state PC (i.e. negative intrusive thoughts) or implicit state PC (i.e. automatic vigilance) additionally predicted delayed cardiac recovery. Fifty-nine participants performed a stressful task, which consisted of an unsolvable synonym task. After a 6-minute recovery period, participants reported on their level of negative intrusive thoughts (i.e. explicit state PC), and performed a lexical decision task (LDT) to measure automatic vigilance for task-related information (i.e. implicit state PC). Cardiac activity was continuously measured using heart rate (HR) and heart rate variability (HRV). Trait worry and rumination were measured by the Penn State Worry Questionnaire (PSWQ) and the Ruminative Response Scale (RRS), respectively. The results showed that high trait worriers had a slower HR recovery from the cognitive stressor compared to low trait worriers. They also showed delayed HRV recovery, but only when the tendency to dwell upon one's negative mood (the 'brooding' subscale of the RRS) was low. Slow HR recovery was associated with high levels of negative intrusive thoughts and with automatic vigilance, but in the unexpected direction for the latter. These results provide evidence that delayed cardiac recovery is associated with trait as well as state PC, and suggest that brooding attenuates the HRV suppressing effect of high trait worry.

Objectives: Psychobiological sensitization and health worry appear to be involved in the etiology of clinical manifestations of subjective health complaints (SHCs) via amplified processing of health-related information. However, it is not clear whether sensitization and health worry are also associated with common SHCs, which are extremely prevalent and are responsible for a large part of both human suffering and health care costs. In this study, we investigated whether SHCs are associated with health worry and two types of sensitization: cognitive health-related sensitization and somatic sensitization. We also examined whether health worry mediates the relationship between cognitive sensitization and SHCs and whether both levels of sensitization interact., Methods: A nonclinical sample of 47 female students completed questionnaires about their recent subjective health as well as health worry and underwent tests for cognitive sensitization, operationalized as Stroop interference and free recall performance, and somatic sensitization, operationalized as pain tolerance and pain threshold in a cold pressor task., Results: Severity of health complaints was positively related with recall of health-related stimuli, but not with Stroop interference, and with worrying about health complaints. In addition, worry mediated the relationship between recall bias and severity of health complaints. Both the number and severity of recent health complaints were associated with pain tolerance. Pain threshold was associated with Stroop interference for health-related information., Conclusions: The results suggest that specific types of cognitive sensitization and somatic sensitization are associated with common health complaints and that worrying about one's complaints might play a role by enhancing biased memory of health-related information.

Perseverative cognition, as manifested in worry and rumination, is a common response to stress, but biopsychological models of stress and health have largely ignored it. These models have generally focused on physiological activation that occurs during stress and have insufficiently addressed effects that occur in anticipation of, or following, stressful events. We argue that perseverative cognition moderates the health consequences of stressors because it can prolong stress-related affective and physiological activation, both in advance of and following stressors. We review evidence that worry, rumination, and anticipatory stress are associated with enhanced cardiovascular, endocrinological, immunological, and neurovisceral activity. The findings yield preliminary support for our hypothesis, suggesting that perseverative cognition might act directly on somatic disease via enhance activation via the cardiovascular, immune, endocrine, and neurovisceral systems.

Several theories of the stress-disease link have now incorporated prolonged activation. This article argues that these theories still lack an important element, that is, the cognitive nature of the mechanism that causes stress responses to be sustained. The perception of stress and the initial response to it do not automatically lead to prolonged activation. The active cognitive representations of stressors need to be prolonged in order to extend their physiological concomitants. We call this mediating process perseverative cognition, and it is manifested in phenomena such as worry, rumination, and anticipatory stress. We summarize evidence suggesting that these phenomena are indeed associated with physiological activation, including cardiovascular, endocrinological and immunological parameters. This evidence is still far from sufficient, due to the many methodological insufficiencies in the studies involved. Nevertheless, it makes clear that cognitive phenomena characterized by perseverative cognition may be likely candidates to mediate the effects of stress sources on somatic disease. We also argue that there is a dearth of evidence supporting the role of prolonged activation. There are a limited number of studies demonstrating prolonged activity related to stressors and emotional episodes, and their methodologies often do not allow unambiguous conclusions. Even more important, the crucial assumption that prolonged activation actually leads to pathogenic states and disease has received hardly any attention yet and therefore is still largely unsupported. There are only a few studies that showed that anticipatory responses and slow recovery from stress predicted disease states.

Sensitization is conceptually related to cognitive bias in experimental psychopathology, and they share the basic mechanism of neuronal sensitization. Every strongly relevant individual concern, like fears, can yield cognitive bias or "cognitive-emotional sensitization". It might also be present for bodily and environmental information related to illness, and could be an etiological factor in medically unexplained complaints. Physiological and cognitive sensitization are theoretically compared. There is evidence for cognitive-emotional sensitization in some medically unexplained somatic complaints, and negative affect is suggested as a catalyst. Prolonged cognitive-emotional sensitization ("perseverative negative cognition" or worry, rumination) might even have demonstrable somatic pathological effects. It is concluded that sensitization may be organized at different levels, both in the organism and in the larger living system within which the organism is subsumed. This view might not only help to clarify medically unexplained pain syndromes, but virtually every subjective complaint, both with and without recognized physiopathology.

Worry postponement, also called stimulus control, is a simple and easy to administer intervention that often forms part of cognitive-behavioural treatments for worry. We conducted a meta-analysis to test if worry postponement is effective in reducing daily worry. Data from 7 randomized trials were included providing a total of 999 participants, of which 250 experienced worry as a burden and of which the majority was women. When comparing worry postponement to the mere registration of worries small effect sizes were observed for worry duration (d = 0.313) and for worry frequency (d = 0.189). Moderation analyses showed that the intervention yielded larger effect sizes in studies including more women. However, long-term follow-up studies are still lacking. Worry postponement, practiced between a week or a maximum of a month, was found to effectively reduce the frequency and duration of worry in daily life. This suggests that a simple intervention is available for people whose worries (temporarily) spiral out of control. [ABSTRACT FROM AUTHOR]

Worry is an important mediator in the relation between stressors and health. This pilot study examined whether a smartphone-based in time worry-reduction training was feasible and improved physiological health (i.e. increased heart rate variability [HRV]). A total of 26 high-worriers were randomised to an experimental or active-control condition (EC and CC respectively). Participants in both conditions registered emotions 5 times daily for a month. The EC additionally received worry-reduction training with mindfulness exercises. Primary outcomes were feasibility and HRV measured at baseline, after 2 weeks (halfway), and at 4 weeks (post-intervention). Both training conditions were feasible and well received. HRV increased in the EC and CC, but this increase did not differ between conditions. Preliminary findings suggest that both training conditions are feasible and might improve HRV, which is an important predictor of cardiovascular disease. This pilot study only provided preliminary evidence, but it laid the groundwork for future randomised controlled trials that ought to include more participants and a waitlist control group in order to get more definitive evidence of the effectiveness of the intervention. [ABSTRACT FROM AUTHOR]

Background: Prolonged cardiac activity that exceeds metabolic needs can be detrimental for somatic health. Psychological stress could result in such "additional cardiac activity."Purpose: In this study, we examined whether prolonged additional reductions in heart rate variability (AddHRVr) can be measured in daily life with an algorithm that filters out changes in HRV that are purely due to metabolic demand, as indexed by movement, using a brief calibration procedure. We tested whether these AddHRVr periods were related to worry, stress, and negative emotions.Methods: Movement and the root of the mean square of successive differences (RMSSD) in heart rate were measured during a calibration phase and the subsequent 24 h in 32 participants. Worry, stress, explicit and implicit emotions were assessed hourly using smartphones. The Levels of Emotional Awareness Scale and resting HRV were used to account for individual differences. During calibration, person-specific relations between movement and RMSSD were determined. The 24-h data were used to detect prolonged periods (i.e., 7.5 min) of AddHRVr.Results: AddHRVr periods were associated with worrying, with decreased explicit positive affect, and with increased tension, but not with the frequency of stressful events or implicit emotions. Only in people high in emotional awareness and high in resting HRV did changes in AddHRVr covary with changes in explicit emotions.Conclusions: The algorithm can be used to capture prolonged reductions in HRV that are not due to metabolic needs. This enables the real-time assessment of episodes of potentially detrimental cardiac activity and its psychological determinants in daily life. [ABSTRACT FROM AUTHOR]

Background: Prolonged physiological activation before or after stressors has gained recognition as a decisive element in theories that explain the link between stress and disease, specifically cardiovascular (CV) disease. This view is opposed to the conventional reactivity hypothesis that emphasizes responses during stressors. Purpose: Prolonged activity has not often been an explicit research goal of real-life stress studies. Nevertheless, a growing number of these studies have provided evidence for prolonged activity, often as a secondary research goal. Methods: An overview of this evidence is lacking and is provided in this article. Results: The combined data from the reviewed studies suggest that discrete and chronic stress sources, as well as negative emotional episodes and dispositions, are related to prolonged CV activity of various durations, including sleep periods. On the other hand, evidence supporting the assumption that prolonged stress-related activation predicts disease is still very modest. Conclusions: In this article we suggest that future research of prolonged activation should give priority to (a) the establishment of clear beginnings and endings of stressful events, (b) the prediction of disease by prolonged activation, and (c) potential psychological mediators of stress-related prolonged activation. These mediators may include, for example, worry and rumination, or other processes characterized by perseverative cognition, including unconscious processes. [ABSTRACT FROM AUTHOR]

Stress, whether daily stress, work stress or traumatic stress, is unhealthy. This lecture covers three recent theoretical approaches in explaining the mechanisms underlying the influence of psychological stress on somatic health. It is argued that stress research should focus less on stressors themselves and put more emphasis on prolonged stress responses. Three mechanisms are identified that cause this unhealthy prolonged stress response: first, the partly-proven mechanism of perseverative cognition; second, the mechanism of unconscious stress, which is currently being explored; and third, the notion of the stress response being a default response that is inhibited only when safety is perceived. All three mechanisms are deeply rooted in millions of years of our evolution. Although the dangers of the past have virtually disappeared, many of us remain ever at the ready for events that never happen. [ABSTRACT FROM AUTHOR]

Abstract: This study examined the psychological processes that may impede or facilitate cardiovascular recovery. It was hypothesized that cardiovascular recovery would be hampered by negative affect and rumination, and facilitated by positive affect. In an experimental study, stress was elicited by exposing participants (N =110) to a mental arithmetic task with harassment. After the stress task, affective levels were manipulated via a movie scene with negative, neutral, or positive emotional valence, or without an affect manipulation (control condition). During the entire experiment, heart rate and systolic and diastolic blood pressure levels were measured continuously. Results indicated that blood pressure recovery was hampered by the negative affect manipulation and by rumination. However, the positive affect manipulation did not facilitate blood pressure recovery. No effects were found on heart rate recovery. In sum, the findings emphasize the importance of negative affect and rumination in stress recovery. [Copyright &y& Elsevier]

Background: Depression is a major risk factor for cardiovascular disease. An important risk factor for cardiovascular disease, low heart rate variability, often has been found in depressed patients and has been associated with impulsivity. The present study investigated whether experimental lowering of serotonin would decrease heart rate variability and increase impulsivity in remitted depressed patients, in particular in those patients with disturbed impulse control. Methods: Nineteen patients in remission from depression received high-dose and low-dose acute tryptophan depletion in a randomized, counterbalanced, double-blind crossover design. Heart rate variability and impulsivity were assessed during each acute tryptophan depletion session and during a baseline session. Suicidal ideation during past depression was used as an index for individual differences in impulse control. Results: High-dose acute tryptophan depletion led to a larger increase in depressive symptoms than did low-dose acute tryptophan depletion. High-dose acute tryptophan depletion decreased heart rate variability and increased impulsivity and anxiety, but only in patients with a history of suicidal ideation. Symptom effects of high-dose acute tryptophan depletion correlated with low heart rate variability at baseline. Conclusions: Depressed patients who have problems with controlling impulsivity might be more at risk for developing cardiovascular disease, possibly related to increased vulnerability to impaired 5-hydroxytryptamine function. [Copyright &y& Elsevier]

Abstract: This study investigated the effects of a compressed working week with high cognitive and emotional work demands within the population of Dutch Helicopter Emergency Medical Service (HEMS) pilots. Work stressors were measured and levels of well-being were examined before, during and after a series of day and night shifts. Results revealed that (i) the start of a series of day shifts was more taxing for well-being than the start of a series of night shifts, (ii) there were no differences in the decrease in well-being during day and night shifts, (iii) distress during shifts was more strongly related to a decrease in well-being during night than during day shifts and (iv) it took HEMS pilots more time to recover from a series of night shifts than from a series of day shifts. It is concluded that HEMS pilots should not start earlier during day shifts, nor have longer series of night shifts. [Copyright &y& Elsevier]