Ten Surprising Facts About Stressful Life Events and Disease Risk

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Abstract

After over 70 years of research on the association between stressful life events and health, it is generally accepted that we have a good understanding of the role of stressors in disease risk. In this review, we highlight that knowledge but also emphasize misunderstandings and weaknesses in this literature with the hope of triggering further theoretical and empirical development. We organize this review in a somewhat provocative manner, with each section focusing on an important issue in the literature where we feel that there has been some misunderstanding of the evidence and its implications. Issues that we address include the definition of a stressful event, characteristics of diseases that are impacted by events, differences in the effects of chronic and acute events, the cumulative effects of events, differences in events across the life course, differences in events for men and women, resilience to events, and methodological challenges in the literature. Expected final online publication date for the Annual Review of Psychology Volume 70 is January 4, 2019. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

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Most cited references 69

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Cognition and depression: current status and future directions.

Ian Gotlib, Jutta Joormann (2010)

Cognitive theories of depression posit that people's thoughts, inferences, attitudes, and interpretations, and the way in which they attend to and recall information, can increase their risk for depression. Three mechanisms have been implicated in the relation between biased cognitive processing and the dysregulation of emotion in depression: inhibitory processes and deficits in working memory, ruminative responses to negative mood states and negative life events, and the inability to use positive and rewarding stimuli to regulate negative mood. In this review, we present a contemporary characterization of depressive cognition and discuss how different cognitive processes are related not only to each other, but also to emotion dysregulation, the hallmark feature of depression. We conclude that depression is characterized by increased elaboration of negative information, by difficulties disengaging from negative material, and by deficits in cognitive control when processing negative information. We discuss treatment implications of these conclusions and argue that the study of cognitive aspects of depression must be broadened by investigating neural and genetic factors that are related to cognitive dysfunction in this disorder. Such integrative investigations should help us gain a more comprehensive understanding of how cognitive and biological factors interact to affect the onset, maintenance, and course of depression.

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Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

Alan Rozanski, James Blumenthal, Jay A. Kaplan (1999)

Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis. Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys. Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. When they do so, the resultant risk for cardiac events is often substantially elevated, equaling that associated with previously established risk factors for CAD, such as hypertension and hypercholesterolemia.

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Psychological stress and cardiovascular disease.

Joel E. Dimsdale (2008)

There is an enormous amount of literature on psychological stress and cardiovascular disease. This report reviews conceptual issues in defining stress and then explores the ramifications of stress in terms of the effects of acute versus long-term stressors on cardiac functioning. Examples of acute stressor studies are discussed in terms of disasters (earthquakes) and in the context of experimental stress physiology studies, which offer a more detailed perspective on underlying physiology. Studies of chronic stressors are discussed in terms of job stress, marital unhappiness, and burden of caregiving. From all of these studies there are extensive data concerning stressors' contributions to diverse pathophysiological changes including sudden death, myocardial infarction, myocardial ischemia, and wall motion abnormalities, as well as to alterations in cardiac regulation as indexed by changes in sympathetic nervous system activity and hemostasis. Although stressors trigger events, it is less clear that stress "causes" the events. There is nonetheless overwhelming evidence both for the deleterious effects of stress on the heart and for the fact that vulnerability and resilience factors play a role in amplifying or dampening those effects. Numerous approaches are available for stress management that can decrease patients' suffering and enhance their quality of life.

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Author and article information

Journal

Title: Annual Review of Psychology

Abbreviated Title: Annu. Rev. Psychol.

Publisher: Annual Reviews

ISSN (Print): 0066-4308

ISSN (Electronic): 1545-2085

Publication date Created: June 27 2018

Publication date Created: January 04 2019

Publication date (Electronic): June 27 2018

Publication date (Print): January 04 2019

Volume: 70

Issue: 1

Affiliations

[1 ]Department of Psychology, Carnegie Mellon University, Pittsburgh, PAennsylvania 15213, USA;,

[2 ]Department of Psychiatry, University of California, San Francisco, California 94118, USA;

Article

DOI: 10.1146/annurev-psych-010418-102857

SO-VID: 5f0780c4-e461-4219-acd6-ba291eac7562

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ScienceOpen disciplines: Medicine,Nutrition & Dietetics,Cardiovascular Medicine,Clinical Psychology & Psychiatry,Public health

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ScienceOpen disciplines: Medicine, Nutrition & Dietetics, Cardiovascular Medicine, Clinical Psychology & Psychiatry, Public health

Ten Surprising Facts About Stressful Life Events and Disease Risk

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Most cited references 69

Cognition and depression: current status and future directions.

Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

Psychological stress and cardiovascular disease.

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