Types of stressors that increase susceptibility to the common cold in healthy adults.

Cohen, Sheldon; Frank, Ellen; Doyle, William J.; Skoner, David P.; Rabin, Bruce S.; Gwaltney, Jack M.

doi:10.1037/0278-6133.17.3.214

Cited by 424 publications

(332 citation statements)

References 30 publications

(67 reference statements)

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“…A series of studies have shown that chronic stress is associated with increased susceptibility to developing a common cold among persons experimentally exposed to an upper respiratory virus (e.g., refs. [14][15][16][17]. This association has been replicated in cross-sectional and prospective studies conducted in natural settings (18).…”

mentioning

confidence: 56%

Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk

Cohen

Janicki-Deverts

Doyle

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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We propose a model wherein chronic stress results in glucocorticoid receptor resistance (GCR) that, in turn, results in failure to downregulate inflammatory response. Here we test the model in two viral-challenge studies. In study 1, we assessed stressful life events, GCR, and control variables including baseline antibody to the challenge virus, age, body mass index (BMI), season, race, sex, education, and virus type in 276 healthy adult volunteers. The volunteers were subsequently quarantined, exposed to one of two rhinoviruses, and followed for 5 d with nasal washes for viral isolation and assessment of signs/symptoms of a common cold. In study 2, we assessed the same control variables and GCR in 79 subjects who were subsequently exposed to a rhinovirus and monitored at baseline and for 5 d after viral challenge for the production of local (in nasal secretions) proinflammatory cytokines (IL-1β, TNF-α, and IL-6). Study 1: After covarying the control variables, those with recent exposure to a long-term threatening stressful experience demonstrated GCR; and those with GCR were at higher risk of subsequently developing a cold. Study 2: With the same controls used in study 1, greater GCR predicted the production of more local proinflammatory cytokines among infected subjects. These data provide support for a model suggesting that prolonged stressors result in GCR, which, in turn, interferes with appropriate regulation of inflammation. Because inflammation plays an important role in the onset and progression of a wide range of diseases, this model may have broad implications for understanding the role of stress in health.lymphocytes | receptor sensitivity | psychological stress | cortisol | hypothalamic-pituitary-adrenocortical axis

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mentioning

confidence: 56%

Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk

Cohen

Janicki-Deverts

Doyle

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

1,026

782

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“…Negative life events-Intuitively, it might not seem reasonable to expect symptoms of mania, such as euphoria, elevated self-esteem, and increased productivity, to follow negative life events. It is worth considering, though, that severe stressors have been found to promote a broad array of psychiatric and physical outcomes, including episodes of schizophrenia (Day, 1989), common colds (Cohen et al, 1998), and ulcers (Gilligan, Fung, Piper, & Tennant, 1987). Given the diversity of outcomes triggered by negative life events, it may not be so unreasonable to expect that life stress could induce mania as well.…”

Section: Life Events and Maniamentioning

confidence: 99%

Life events in bipolar disorder: Towards more specific models

Johnson

2005

Clinical Psychology Review

180

167

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This article reviews the evidence concerning life events as a predictor of symptoms within bipolar disorder. First, key methodological issues in this area are described, and criteria used for including studies in this review are defined. Then findings that negative life events predict worse outcomes within bipolar disorder are reviewed. Beyond general studies on relapse, it is important to differentiate predictors of depression from predictors of mania. When severe negative life events occur, they appear to trigger increases in bipolar depression. Nonetheless, many depressions are unrelated to negative life events and appear to be triggered by other variables. The strongest evidence suggests that negative life events do not trigger mania, except perhaps in certain contexts. Retrospective findings for schedule-disrupting life events as a trigger for manic symptoms await further assessment within a longitudinal study. Life events involving goal attainment do appear to trigger manic symptoms. Overall, it is time to differentiate among specific types of life events, as these different forms of events point towards mechanisms linking stressors with symptom expression. These mechanisms provide clues into ways to integrate the social environment with biological vulnerability (see Bipolar disorder is clearly a biological disorder. Nonetheless, over the past 15 years, a wealth of research has made it abundantly clear that psychosocial variables shape outcomes of this disorder. Much of this psychosocial research has focused on whether life events predict the timing and severity of symptoms within this disorder. This paper reviews the evidence that life events are related to symptom expression within bipolar disorder. This basic question has challenged researchers for over 20 years. Given the growing literature, this paper focus on addressing two more specific questions. Which types of symptoms are related to life events? What types of life events influence symptoms? Given the growing number of studies available on these issues, this review will focus on those studies with the most rigorous methodologies. To set the stage for this endeavor, it is important to first review the major methodological issues in research on life events and bipolar disorder, including issues related to design, measurement, and sampling.

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“…In 1884, the editor of the British Medical Journal noted that at funerals "the depression of spirits under which the chief mourners labour at these melancholy occasions peculiarly predisposes them to some of the worst effects of the chill" [1]. Since then, morbidity has been shown to be significantly increased during chronic stress in both observational [2][3][4][5] and live virus challenge [6][7][8][9] studies. These provide compelling evidence that psychological stress is associated with an impairment of the immune system's ability to respond to infection.…”

Section: Introductionmentioning

confidence: 99%

Antibody response to vaccination and psychosocial stress in humans: relationships and mechanisms

Burns

Carroll

Ring

et al. 2003

Vaccine

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The purpose of this review is to determine the effects of psychosocial stress on antibody response to vaccination in humans, consider possible mechanisms, and identify agenda for future research. Studies of the association between stress and vaccination response in humans were reviewed. There is evidence of a negative association between stress and antibody response to vaccination, which is most apparent with thymusdependent vaccines and when measured at extended times after vaccination. Preliminary findings implicate the hypothalamic-pituitary-adrenal axis and sympathetic nervous system as potential mechanisms, although a role for unhealthy behaviours cannot be discounted at this stage. Results to date are sufficiently indicative to direct future research to untangling their theoretical ramifications, as well as realising their clinical implications.

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Types of stressors that increase susceptibility to the common cold in healthy adults.

Cited by 424 publications

References 30 publications

Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk

Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk

Life events in bipolar disorder: Towards more specific models

Antibody response to vaccination and psychosocial stress in humans: relationships and mechanisms

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