Association of depression with medical illness: does cortisol play a role?

Brown, E. Sherwood; Varghese, Femina P.; McEwen, Bruce S.

doi:10.1016/s0006-3223(03)00473-6

Cited by 504 publications

(308 citation statements)

References 120 publications

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“…Under these circumstances, "allostatic load" on the body increases, placing physical health at risk (McEwen, 1998(McEwen, , 2008. For example, persistent exposure to cortisol and other stress hormones can negatively affect bone density, increase blood pressure, promote atherosclerotic changes in arteries, and increase the risk of myocardial infarction (Brown, Varghese, & McEwen, 2004). Musculoskeletal ailments have also been associated with another form of allostatic loaddHPA axis hyporesponsivenessdwherein low cortisol responses to stress allow increased secretion of inflammatory cytokines that promote autoimmune and other inflammatory diseases, many of which affect the musculoskeletal system (Boscarino, 2004;McEwen, 1998).…”

Section: Linking Psychological Stress and Physical Healthmentioning

confidence: 99%

Health status and health care utilization following collective trauma: A 3-year national study of the 9/11 terrorist attacks in the United States

Holman

Silver

2011

Social Science & Medicine

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a b s t r a c tThe September 11, 2001 terrorist attacks (9/11) presented a unique opportunity to assess the physical health impact of collective stress in the United States. This study prospectively examined rates of physical ailments and predictors of health care utilization in a U.S. nationally representative sample over three years following the attacks. A sample of adults (N ¼ 2592) completed a survey before 9/11/01 that assessed MD-diagnosed physical and mental health ailments. Follow-up surveys were administered at one (N ¼ 1923), two (N ¼ 1576), and three (N ¼ 1950) years post-9/11 to assess MD-diagnosed physical health ailments (e.g., cardiovascular, endocrine) and health care utilization. Reports of physical ailments increased 18% over three years following 9/11. 9/11-related exposure, lifetime and post-9/11 stress, MD-diagnosed depression/anxiety, smoking status, age, and female gender predicted increased incidence of post-9/11 ailments, after controlling for pre-9/11 health. After adjusting for covariates (demographics, somatization, smoking status, pre-9/11 mental and physical health, lifetime and post-9/11 stress, and degree of 9/11-related exposure), increases in MD-diagnosed cardiovascular, endocrine, gastrointestinal, and hematology-oncology ailments predicted greater utilization of health care services over two years. After the collective stress of 9/11, rates of physical ailments increased and predicted greater health care utilization in a U.S. national sample.

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Section: Linking Psychological Stress and Physical Healthmentioning

confidence: 99%

Health status and health care utilization following collective trauma: A 3-year national study of the 9/11 terrorist attacks in the United States

Holman

Silver

2011

Social Science & Medicine

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“…Whilst a number of studies have reported increased basal plasma cortisol levels in a subset of depressed patients relative to matched controls (Brown et al, 2004), there is also evidence for decreased plasma cortisol in depression and other stress-related disorders (Silverman and Sternberg, 2012). Another rationale for studying adrenal/corticosterone status is the evidence that stress can induce glucocorticoid resistance which in turn results in attenuation of its anti-inflammatory function (Rhen and Cidlowski, 2005;Silverman and Sternberg, 2012).…”

Section: Introductionmentioning

confidence: 99%

Mouse social stress induces increased fear conditioning, helplessness and fatigue to physical challenge together with markers of altered immune and dopamine function

et al. 2014

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In neuropsychiatry, animal studies demonstrating causal effects of environmental manipulations relevant to human aetiology on behaviours relevant to human psychopathologies are valuable. Such valid models can improve understanding of aetio-pathophysiology and preclinical discovery and development of new treatments. In depression, specific uncontrollable stressful life events are major aetiological factors, and subsequent generalized increases in fearfulness, helplessness and fatigue are core symptoms or features. Here we exposed adult male C57BL/6 mice to 15-day psychosocial stress with loss of social control but minimal physical wounding. One cohort was assessed in a 3-day test paradigm of motor activity, fear conditioning and 2-way avoid-escape behaviour on days 16-18, and a second cohort was assessed in a treadmill fatigue paradigm on days 19 and 29, followed by the 3-day paradigm on days 30-32. All tests used a physical aversive stimulus, namely mild, brief electroshocks. Socially stressed mice displayed decreased motor activity, increased fear acquisition, decreased 2-way avoid-escape responding (increased helplessness) and increased fatigue. They also displayed increased plasma TNF and spleen hypertrophy, and adrenal hypertrophy without hyper-corticoidism. In a third cohort, psychosocial stress effects on brain gene expression were assessed using next generation sequencing. Gene expression was altered in pathways of inflammation and G-protein coupled receptors in prefrontal cortex and amygdala; in the latter, expression of genes important in dopamine function were de-regulated including down-regulated Drd2, Adora2a and Darpp-32. This model can be applied to identify targets for treating psychopathologies such as helplessness or fatigue, and to screen compounds/biologics developed to act at these targets. AbstractIn neuropsychiatric research, animal studies that demonstrate causal effects of environmental manipulations relevant to human aetiological factors on emotional and cognitive behaviours relevant to human psychopathologies are valuable. Such valid animal models can be useful for improved understanding of aetio-pathophysiology and preclinical discovery and development of new treatments. In depression, specific uncontrollable stressful life events are major aetiological factors, and subsequent generalized increases in fearfulness, helplessness and fatigue are core psychopathology symptoms or features. In the present study we exposed adult male C57BL/6 mice to an environmental manipulation of 15-day psychosocial stress with loss of social control but with minimal physical wounding. One cohort of stressed and control mice was assessed in a novel 3-day test paradigm of motor activity, fear conditioning and 2-way avoid-escape behaviour on days 16-18, and a second cohort was assessed in a treadmill fatigue paradigm on days 19 and 29, followed by the 3-day paradigm on days 30-32. All tests used a physical aversive stimulus, namely mild, brief electroshocks. The socially stressed mice displayed dec...

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“…(Musselman, Evans, & Nemeroff, 1998). Abnormal HPA-axis function may contribute to CVD risk through a variety of related risk factors, including hypertension, high lipids, insulin resistance, and abdominal obesity, together constituting the metabolic syndrome (Brown, Varghese, & McEwen, 2004). Several studies have reported basal hypercortisolism (e.g., Gotthardt et al, 1995;Plotsky, Owens, & Nemeroff, 1998), hypercortisolism in response to stress (for a review, see Burke, Davis, Otte, & Mohr, 2005), or elevated cortisol levels after awakening in depression (e.g., Bhagwagar, Hafizi, & Cowen, 2005).…”

Section: Introductionmentioning

confidence: 99%

Circadian affective, cardiopulmonary, and cortisol variability in depressed and nondepressed individuals at risk for cardiovascular disease

Conrad

Wilhelm

Roth

et al. 2008

Journal of Psychiatric Research

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Depression is a risk factor for cardiovascular disease (CVD) perhaps mediated by hypothalamicpituitary-adrenal (HPA) axis or vagal dysregulation. We investigated circadian mood variation and HPA-axis and autonomic function in older (≥55 years) depressed and nondepressed volunteers at risk for CVD by assessing diurnal positive and negative affect (PA, NA), cortisol, and cardiopulmonary variables in 46 moderately depressed and 19 nondepressed volunteers with elevated CVD risk. Participants sat quietly for 5-min periods (10:00, 12:00, 14:00, 17:00, 19:00, 21:00), and then completed an electronic diary assessing PA and NA. Traditional and respiration-controlled heart rate variability (HRV) variables were computed for these periods as an index of vagal activity. Salivary cortisols were collected at waking, waking+30 min, 12:00, 17:00, and 21:00 hours. Cortisol peaked in the early morning after waking, and gradually declined over the day, but did not differ between groups. PA was lower and NA was higher in the depressed group throughout the day. HRV did not differ between groups. Negative emotions were inversely related to respiratory sinus arrhythmia in nondepressed participants. We conclude that moderately depressed patients do not show abnormal HPA-axis function. Diurnal PA and NA distinguish depressed from nondepressed patients at risk for CVD, while measures of vagal regulation, even when controlled for physical activity and respiratory confounds, do not. Diurnal mood variations of older individuals at risk for CVD differ from those reported for other groups and daily fluctuations in NA are not related to cardiac autonomic control in depressed individuals. KeywordsCardiovascular Disease; Cortisol; Depression; Heart Rate Variability Depression has a major impact on mortality, morbidity, and functional recovery in patients with cardiovascular disease (CVD) (Carney, Freedland, & Sheps, 2004). Several mechanisms have been proposed to explain how depression might increase CVD risk, including Corresponding Author: Frank H. Wilhelm, Ph.D.; Tel.: ++41-61-267 0593; Fax: ++41-61-267 0659; E-mail: frank.wilhelm@unibas.ch; Address: Institute for Psychology, University of Basel, Missionsstrasse 60/62, CH-4055 Basel, Switzerland. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. (Musselman, Evans, & Nemeroff, 1998). Abnormal HPA-axis function may contribute to CVD risk through a variety of related risk factors, including hypertension, high lipids, insulin resistance, and abdominal obesity, together constituting the metabolic syndrome (Brown, Varghese, & McEwen, 2004). Several stu...

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Association of depression with medical illness: does cortisol play a role?

Cited by 504 publications

References 120 publications

Health status and health care utilization following collective trauma: A 3-year national study of the 9/11 terrorist attacks in the United States

Health status and health care utilization following collective trauma: A 3-year national study of the 9/11 terrorist attacks in the United States

Mouse social stress induces increased fear conditioning, helplessness and fatigue to physical challenge together with markers of altered immune and dopamine function

Circadian affective, cardiopulmonary, and cortisol variability in depressed and nondepressed individuals at risk for cardiovascular disease

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