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Depressive Symptoms Are Associated With Blunted Cortisol Stress Responses in Very Low-Income Women
Abstract
The purpose of this study was to examine the association between depressive symptoms and salivary cortisol responses to stress in a high-risk population of very poor Mexican women.
Adult women (N = 1109) between the ages of 18 and 44 years (mean age, 29) were identified in a house-to-house survey in low-income areas (income <20th percentile nationally) of urban Mexico. An interview containing the Spanish version of the Center for Epidemiologic Studies--Depression Scale (CES-D) was administered to all women. The naturalistic stressor was defined as the unexpected arrival of a team of researchers at the participants' homes followed by an in-depth interview and physical assessment, with saliva samples taken at time of arrival (baseline), 25 minutes, and 50 minutes after arrival.
The mean CES-D score was 19.42 (range, 0-53). Results of hierarchical linear modeling analyses revealed no effect of depressive symptoms on baseline salivary cortisol levels. However, a significant depressive symptom by time interaction revealed that women with elevations in depressive symptoms (CES-D scores = 35) failed to exhibit a cortisol response to the stressor. In contrast, in women with lower CES-D scores, cortisol levels significantly increased in response to the stressor.
Consistent with research on individuals with major depressive disorder, results of this study demonstrate that women with very high levels of depressive symptoms exhibit blunted cortisol responses to a naturalistic psychological stressor. Results also contribute to previous research by generalizing findings to a high risk, underserved population of women.
... Inability to properly regulate aspects of these responses has been proposed as an essential factor in the pathophysiology of various stress-related disorders, including depression [3]. Indeed, evidence from the literature indicates that depression is linked to alterations in neuroendocrine responses to mental stress, more specifically alterations in cortisol and norepinephrine responses, which can be related to increased risk of cardiovascular disease (CVD) [2,[4][5][6][7]. Depression has been associated with increases in norepinephrine responses to stress [8]. ...
... A recent study by Hamer and Malan [6] supported the link between depressive symptoms, norepinephrine responses and metabolic syndrome in black Africans [6]. There remains no clearcut nor generally accepted model for cortisol responses in depression, as both blunted and increased cortisol activity have previously been noted [5,[9][10][11]. To our knowledge, no study has yet attempted to investigate the association between depressive symptoms, neuroendocrine responses and increased cardiovascular risk [left ventricular hypertrophy (LVH)] in black Africans. ...
... Blunted cortisol responses to laboratory and naturalistic psychosocial stressors have been demonstrated in both clinical and subclinical depression [36,37]. For instance, Burke et al. [5] demonstrated that women with high depressive symptoms exhibited blunted cortisol stress responses to a naturalistic stressor [5]. This response is possibly not unexpected as depression is typically associated with elevated cortisol, while at the same time demonstrating a blunted response to dexamethasone challenge [1,38,39]. ...
Objective Chronic psychosocial stress as experienced in an urban environment plays an important role in the aetiology of depression-related cardiovascular risk. It is uncertain whether acute mental stress responses aggravate this risk. Therefore, we aimed to explore the associations between depressive symptoms, neuroendocrine acute mental stress responses and cardiovascular risk, that is ECG-left ventricular hypertrophy (ECG-LVH), in a black South African cohort. Materials and methods The substudy sample consisted of 179 black African men and women from the Sympathetic Activity and Ambulatory Blood Pressure in Africans study. Depressive symptoms were evaluated using the nine-item Patient Health Questionnaire and the participants were stratified into black Africans with depressive symptoms and without. Cortisol and 3-methoxy-phenylglycol (MHPG) responses were analysed during rest and exposure to the Stroop mental stressor. Cortisol median split responses were determined and stratified sex groups accordingly into above (>1.5 ng/ml) and below (≤1.5 ng/ml) responders. Blood pressure and ECG-LVH data were obtained from 24-h ambulatory monitoring and 12-lead ECG. Results The Africans with depressive symptoms demonstrated mean hypertensive status, blunted cortisol and MHPG acute mental stress responses (P≤0.05). In Africans with depressive symptoms and low cortisol stress responses, blunted MHPG acute mental stress responses were associated with ECG-LVH in Africans [adjusted R2=0.20; β=0.92 (95% confidence interval 0.74, 1.10); P≤0.02]. Conclusion Blunted neuroendocrine responses were linked to depressive symptoms and ECG-LVH in black Africans. When coupled to their hypertensive status, these vasoconstrictive agent responses may underpin the increased long-term depression and vascular disease risk in urban Africans.
... Some researchers have found that lower levels of cortisol have been associated with chronic stress, and depression (Burke, Fernald, Gertler, and Adler, 2005;Zarkovic et al., 2003), while others have demonstrated that stress, anxiety, and depression are associated with higher levels of salivary cortisol (van Eck et al., 1996). These inconsistencies may be the result of the variety of way and methods used to analyze salivary cortisol. ...
... These inconsistencies may be the result of the variety of way and methods used to analyze salivary cortisol. Some researchers use morning cortisol levels or morning area under the curve, while other use multi-level analyses to estimate the average cortisol levels over time (Burke et al., 2005;Kirschbaum and Hellhammer, 1994). In addition to differences in statistical methodology, the settings in which salivary cortisol is collected also differ. ...
... In addition to differences in statistical methodology, the settings in which salivary cortisol is collected also differ. For example, Burke and colleagues (2005) (Burke et al., 2005;Zarkovic et al., 2003); where as elevated evening cortisol levels have been associated with cardiovascular disease (Stewart and Seeman, 2000). More research is needed to resolve these methodological issues. ...
... Collectively, these findings in healthy individuals suggest that stress (and associated cortisol release) decreases connectivity between limbic and prefrontal circuits, interrupting top-down control. However, cortisol response to stress is blunted in MDD (18), particularly in females (19), which may result in maladaptive responses in stress circuitry, although this relationship is unexplored. Critically, in individuals with current or remitted MDD (rMDD), acute stress induction was found to reduce activation in the ventromedial prefrontal cortex (vmPFC) (20). ...
... Conversely, the clinical groups had higher activation in the evaluative SN and the stress-related network (Temp-Ins-Amyg), suggesting exaggerated bottom-up threat signaling. Similar to previous findings (19), we observed a blunted cortisol response to stress in individuals with MDD and lower cortisol response in females compared with males. The reduced cortisol response in MDD seems to be state-dependent, and higher cortisol response in rMDD may be an important biological marker of remission, potentially representing a reengagement of emotional responding, which can be blunted in MDD (37). ...
Objective:
Preclinical work suggests that excess glucocorticoids and reduced cortical γ-aminobutyric acid (GABA) may affect sex-dependent differences in brain regions implicated in stress regulation and depressive phenotypes. The authors sought to address a critical gap in knowledge, namely, how stress circuitry is functionally affected by glucocorticoids and GABA in current or remitted major depressive disorder (MDD).
Methods:
Multimodal imaging data were collected from 130 young adults (ages 18-25), of whom 44 had current MDD, 42 had remitted MDD, and 44 were healthy comparison subjects. GABA+ (γ-aminobutyric acid and macromolecules) was assessed using magnetic resonance spectroscopy, and task-related functional MRI data were collected under acute stress and analyzed using data-driven network modeling.
Results:
Across modalities, trait-related abnormalities emerged. Relative to healthy comparison subjects, both clinical groups were characterized by lower rostral anterior cingulate cortex (rACC) GABA+ and frontoparietal network amplitude but higher amplitude in salience and stress-related networks. For the remitted MDD group, differences from the healthy comparison group emerged in the context of elevated cortisol levels, whereas the MDD group had lower cortisol levels than the healthy comparison group. In the comparison group, frontoparietal and stress-related network connectivity was positively associated with cortisol level (highlighting putative top-down regulation of stress), but the opposite relationship emerged in the MDD and remitted MDD groups. Finally, rACC GABA+ was associated with stress-induced changes in connectivity between overlapping default mode and salience networks.
Conclusions:
Lifetime MDD was characterized by reduced rACC GABA+ as well as dysregulated cortisol-related interactions between top-down control (frontoparietal) and threat (task-related) networks. These findings warrant further investigation of the role of GABA in the vulnerability to and treatment of MDD.
... (DSM-5) states, depression is characterized by sadness, feeling of loneliness or ill-tempered mood [6]. Among the 3 types of depression (mild, moderate and major), a person having Major Depressive Episode (MDE) presents with complaints of mood disturbance and the person feels disheartened, dejected and useless [7]. In MDE, these symptoms are prolonged and persist for more than 2-weeks. ...
... These results are in consistent with a study carried out by Herbert, et al., [11]. They found a higher level of cortisol in saliva in major depression illness individuals [7]. A remarkable relationship between salivary cortisol and depression was also observed by Yonekura, et al., [16]. ...
Introduction: This study compared the levels of salivary cortisol in patients suffering from severe depression and in healthy individuals. Methods: Sample size included 30 diagnosed cases of major depression based on outdoor clinical assessment (from April 2015 to December 2105) and was established by ICD-10 and DSM-IV criteria and 30 physically and mentally healthy subjects. In this study diagnosed cases of hyperaldosteronism, Cushing's syndrome/ disease were omitted. A predesigned proforma was created on the basis of Becks Inventory. Saliva samples were collected and processed, and the measurement of cortisol levels was done by ELISA. Results: In a normal subject, the mean cortisol level was 1.46 ± 0.9 µg/dl (Mean ± SD) whereas in depressive patients it was raised (2.2 ± 1.6 µg/dl, p=0.031). Results also showed that high level of cortisol in saliva was found in individuals with a positive family history of depression (2.3 ± 1.8 µg/dl) as compared to healthy subjects (1.5 ± 1.0 µg/dl). Mean BMI was also found to be different between the 2 groups (p=0.012). Conclusion: We concluded that salivary cortisol may act as an early diagnostic tool and non-invasive biomarker for prompt diagnosis of potential cases of depression for effective management. Hence, early initiation of treatment can be helpful in improving the late clinical consequences in severely depressed patients and decreasing the morbidity.
... A further study using a naturalistic stressor consisting of an unexpected visit by health professionals at the home of very low-income Mexican women following an in-depth interview and physical assessment showed that women with more severe depressive symptoms exhibited more blunted cortisol responses to stress than those with less severe symptoms (H. M. Burke, Fernald, Gertler, & Adler, 2005). Authors using a mental arithmetic task revealed that clinically depressed individuals also showed blunted cortisol responses (Trestman et al., 1991). ...
... Thus, if the long-term pattern of increased HPA reactivity persists, one might imagine that this may lead to damage in the long run, resulting in a blunted HPA reactivity, as observed in patients with melancholic depression (H. M. Burke, Fernald et al., 2005). This hypothesis is appropriate, since animal studies showed that there is an initial increase of corticosterone secretion to stress, which is followed by a reduced responsiveness over time (Heim, Ehlert, & Hellhammer, 2000). ...
Eine Schwangerschaft stellt für die meisten Frauen ein einschneidendes Ereignis dar und bedarf diverser physiologischer und psychologischer Anpassungsprozesse. Psychosoziale Belastungen in der Schwangerschaft scheinen diese Anpassungsprozesse, u.a. auf der hormonellen Ebene, in ungünstiger Weise zu beeinflussen und das Risiko für Komplikationen in der Schwangerschaft und bei der Geburt zu erhöhen. Im ersten Teil der vorliegenden Arbeit bestand das Ziel darin, psychosoziale relevante Faktoren, die einen ungünstigen Einfluss auf den Schwanger- und Geburtsverlauf haben können, in einem neuen Messverfahren zu integrieren. Der Fragebogen soll als mögliches Screeninginstrument zur Früherkennung von Frauen mit einem erhöhten psychosozialen Risiko für die Entwicklung von Schwangerschafts- oder Geburtskomplikationen eingesetzt werden können. Anhand von Interviews mit Schwangeren und unter Einbeziehung bestehender Messinstrumente zur Erfassung von Belastungen in der Schwangerschaft, wurden fünf Skalen mit je zehn Items konstruiert: Das Zürcher Inventar zur psychosozialen Befindlichkeit in der Schwangerschaft (ZIPS). In zwei aufeinander folgenden Substudien (N = 154 bzw. N = 60) wurde die interne faktorielle Struktur des ZIPS überprüft und die Reliabilität und Validität untersucht. Insgesamt liefern die vorliegenden Befunde dieser Fragebogenanalyse erste Hinweise auf eine plausible Faktorenstruktur, gute psychometrische Kennwerte und interessante erste Validitätsbefunde. Beim ZIPS handelt es sich um ein psychometrisch solides Verfahren, das die psychosoziale Befindlichkeit von Schwangeren umfassend zu erheben vermag. Dementsprechend könnten anhand eines Screenings Frauen mit einem erhöhten psychosozialen Risiko von einer frühen Intervention präventiver Art profitieren. Im zweiten Teil der Doktorarbeit wurde der Zusammenhang zwischen der psyochobiologischen Stressreaktivität während der gesunden Schwangerschaft und der psychischen Befindlichkeit postpartum untersucht. Hierzu nahmen 57 gesunde Schwangere an einem standardisierten psychosozialen Stresstest (Trier Social Stress Test, TSST) teil. Die biologische Stressreaktivität wurde im Speichel anhand des endokrinen Parameters Cortisol gemessen, während psychologische Faktoren mittels Fragebogen erhoben wurden. Es konnte gezeigt werden, dass Frauen, die nach der Geburt eine depressive Symptomatik (Postpartum Blues) entwickelten, bereits während der Schwangerschaft eine auffällige psychobiologische Stressreaktivität aufwiesen. Frauen mit einer depressiven Gestimmtheit postpartum zeigten im Stresstest höhere Cortisolanstiege, eine höhere Ängstlichkeit und eine schlechtere Befindlichkeit nach der Stresskonfrontation. Zudem wurde bei den Frauen dieser Gruppe generell eine erhöhte Ängstlichkeit und Stressanfälligkeit sowie vermehrt Appetit- und Schlafstörungen festgestellt als bei den Frauen, die nach der Entbindung keine depressive Verstimmung berichteten. Die Ergebnisse weisen darauf hin, dass gesunde Schwangere mit einem erhöhten Risiko für postpartale depressive Verstimmung bereits während der Schwangerschaft anhand einer höheren Cortisolreaktivität und einer höheren psychologischen Reaktivität auf einen psychosozialen Stressor frühzeitig identifiziert werden können. For most women pregnancy represents an incising event and requires various physiological and psychological adaptive processes. Psychosocial stress seems to have adverse impact on these adaptive processes and is known to increase the risk for pregnancy and birth complications. The purpose of the first part within this research project was the development and validation of a new inventory assessing important aspects of the psychosocial well- being during pregnancy. The development of the questionnaire based on interviews with pregnant women as well as on the comprehension of existing instruments measuring pregnancy related psychosocial strain. The development resulted in an inventory consisting of five scales, with ten items each: The Zurich Inventory of Psychosocial Well-being in Pregnancy (ZIPP). In order to investigate its factorial structure the inventory was applied to a sample of 154 pregnant women. The reliability and validity was examined by means of the data of 60 pregnant women. The results show a consistent factorial structure and strongly support good psychometric properties of the scales and validity. Taken together, the findings indicate that the ZIPP is a short psychometric instrument which validly and reliably assesses psychosocial well-being in pregnancy. In regard to the results concerning the predictive validity the questionnaire is applicable as a screening tool helping to identify women at risk for an adverse birth outcome. Thus, the possibility for early preventive intervention is given. The purpose of the second part of this work was to examine the association between psychobiological stress reactivity during healthy pregnancy and depressive symptoms in the early puerperium. A sample of healthy nulliparous pregnant women (N = 57) between the ages of 21 and 35 years underwent a standardized psychosocial stress test (TSST) during pregnancy. Women with depressive symptoms postpartum showed significantly higher cortisol responses to the stress test compared to women without depressive symptoms in the puerperium, whereas baseline levels did not differ. Additionally, women in the depressive group showed significantly higher state anxiety and lower mood state throughout the experiment. Furthermore, women in this group showed higher stress susceptibility, higher trait anxiety and higher levels in the Symptom Checklist. No differences were found for prior episodes of psychiatric disorders, obstetrical complications, birth weight or mode of delivery. Our data provide evidence that healthy pregnant women developing postpartum depressive symptoms might be identified already during pregnancy by means of their higher cortisol reactivity and their higher psychological reactivity in response to psychosocial stress. The higher cortisol stress response might be interpreted as a biological prodromal symptom, preceding postpartum depressive mood changes.
... If this regulatory response is blunted, consequences may include inadequate allocation of energy towards a psychological or behavioral response to the stressor, and may also lead to incomplete physiological restoration that over time can increase allostatic load and vulnerability to illnesses 60,61 . For example, blunted cortisol response to stress is associated with various forms of psychopathology, such as depression 62 , alcohol and substance abuse 63 , and schizophrenia 64 . This is also consistent with evidence from the present study showing that individuals with blunted cortisol response to stress engaged in less effective coping strategies and reported increased cognitive intrusion, which can in turn increase the risk for depression and anxiety (i.e. ...
... Furthermore, this study suggests that a blunted cortisol response is associated with increased cognitive intrusion and avoidance in response to personal stress, and both cognitive intrusion and avoidance have been identified as moderators in the relationship between stress and incident insomnia 67 . Additionally, blunted cortisol response and the associated deficits in coping have also been associated with psychiatric illnesses such as depression 62 , and thus may represent the biological underpinnings of sleep disturbance as a transdiagnostic risk factor. ...
Objectives
Abnormalities in the stress system have been implicated in insomnia. However, studies examining physiological stress regulation in insomnia have not consistently detected differences in the hypothalamic–pituitary–adrenal (HPA)-axis response to stress. One explanation may be that deficits in the stress system are associated specifically with a biological vulnerability to insomnia rather than the phenotypic expression of insomnia. To examine stress response as a function of vulnerability to insomnia, this study tested response to the Trier Social Stress Test in a sample of healthy sleepers with varying familial risk for insomnia.
Methods
Thirty-five healthy individuals with and without familial risk for insomnia were recruited to complete a laboratory stressor. Participants with one or both biological parents with insomnia were categorized as positive for familial risk, whereas those without biological parents with insomnia were categorized as negative for familial risk. Participants completed the Trier Social Stress Test in the laboratory, and psychological and physiological (autonomic and HPA-axis) responses were compared.
Results
Despite self-reported increases in anxiety, those positive for familial risk exhibited a blunted cortisol response relative to those without familial risk for insomnia. Individuals with blunted cortisol also reported heightened reactivity to personal life stressors, including increased sleep disturbances, elevated cognitive intrusions, and more behavioral avoidance.
Conclusions
Findings from this study provide initial evidence that abnormal stress regulation may be a biological predisposing factor conferred via familial risk for insomnia. This deficit may also predict negative consequences over time, including insomnia and the associated psychiatric comorbidities.
... 12,13 Maternal HPA dysregulation can increase the risk for poor maternal postpartum adjustment, which can negatively affect infant health and development. 12,[14][15][16][17][18] The connection between cortisol dysregulation and depressive symptoms has been found among low-income, nonpregnant Mexican American women 19,20 and non-Hispanic white mothers in the postpartum period. 17 A recent study including an ethnically diverse sample of pregnant women found that low socioeconomic status was associated with both elevated perceived stress and elevated levels of cortisol across the day. ...
... We treated postpartum depressive (PPD) symptoms at 6 weeks as a potential confound because prior research supports the association of PPD with maternal stress, social support, and cortisol. 17,19,[33][34][35] Therefore, we adjusted for 6-week depressive symptoms in the prediction of maternal cortisol at 12 weeks. ...
Low-income Mexican American women experience significant health disparities during the postpartum period. Contextual stressors, such as economic stress, are theorized to affect health via dysregulated cortisol output. However, cultural protective factors including strong family support may buffer the impact of stress. In a sample of 322 low-income Mexican American women (mother age 18-42; 82% Spanish-speaking; modal family income 15,000), we examined the interactive influence of economic stress and family support at 6 weeks postpartum on maternal cortisol output (AUCg) during a mildly challenging mother-infant interaction task at 12 weeks postpartum, controlling for 6-week maternal cortisol and depressive symptoms. The interaction significantly predicted cortisol output such that higher economic stress predicted higher cortisol only among women reporting low family support. These results suggest that family support is an important protective resource for postpartum Mexican American women experiencing elevated economic stress.
... The stress exposure model of depression suggests that MDD is the result of a vulnerability to depression, combined with the trigger of stressful life events (Hankin et al., 2007;Liu and Alloy, 2010). Accordingly, psychosocial stressors are among the top reported antecedents to depression episodes (Frank et al., 1994;Kendler et al., 1999;Kendler et al., 2000), and dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis response is a consistent finding in major depression (Burke et al., 2005;Lupien et al., 2009). Psychosocial stress may be especially important in the etiology of mood disorders in women as the depressogenic effects of life stressors are reportedly greater in women than men (Mezulis et al., 2010), even when there is no difference in the number of stressful life events or in the subjective perception of these events (Korszun, 2009). ...
... Estradiol receptors are located in a number of brain areas, including regions important for the autonomic, hormonal, and cognitive-emotional response to psychosocial stress (Love et al., 2010). The relation of stress to depression onset (Frank et al., 1994;Kendler et al., 1999;Kendler et al., 2000) and the altered function of the stress system in major depression (Burke et al., 2005;Lupien et al., 2009) suggest that modulation of the psychosocial stress response may be a mechanism through which estradiol fluctuation may contribute to MDD and PTSD risk. The results of this study suggest that estradiol levels may modulate activity in brain areas important for processing emotional information during psychosocial stress. ...
... The phenomenon of the cortisol awakening response involves a spike in cortisol levels by 50% of the clinical range within 30 min post-awakening; it can often be an indication of irregularities in cortisol responses and dysfunctionality of the HPA axis. For example, in Burke et al. and Huber et al., clinical depression patients presented lower cortisol awakening responses compared to healthy matched controls [16][17][18]. Evidently, the monitoring of cortisol is a useful tool for the determination of psychological and physiological stress levels, as well as any mental health implications such as clinical depression and major depressive disorder [19]. ...
Mental illnesses, such as clinical depression, have taken an unprecedented toll on society and the economy on a global scale. The relationship between stress management and mental health decline is of utmost significance, especially as most avenues of mental health management remain inaccessible for the majority of the general public, i.e., interview-based, and face-to-face interventions or costly drug-based therapies. Cortisol, the primary stress hormone, regulates the stress response in the human body and, through persistent activation, can lead to chronic stress and mental health deterioration. Thereby, the measurement and evaluation of cortisol within saliva could harness potential developments in management and diagnostic tools to monitor physiological and psychological stress in simple point-of-care applications. The current study aims to determine the concentration of salivary cortisol in spiked artificial saliva samples using blue tetrazolium (BT) dye as a colorimetric indicator. The proposed method showcases the use of the BT dye as an effective method for the rapid measurement of salivary cortisol, with accuracy comparable to the gold-standard method for salivary cortisol analysis, enzyme-linked immunoassays (ELISAs). Finally, a prototype colorimetric sensor has been developed for point-of-care applications of stress monitoring via salivary cortisol measurement.
... For example, it is possible that higher HPA-axis reactivity to the TSST indicates an inability of the HPA-axis, as an allostatic system, to adapt to stressful challenges in everyday life. Over time, this pattern of higher reactivity may result in higher baseline levels of cortisol and eventually the blunted HPA reactivity associated with more chronic depressive symptoms (e.g., Burke et al., 2005). This possibility is supported by multiple strands of research, including animal studies demonstrating an initial increase in glucocorticoid secretion to stress, followed by a decreased glucocorticoid response over time (Heim et al., 2000). ...
Background:
Research suggests a link between stress and depression, especially in high-risk groups. The perinatal period is known as a time of increased risk for depression and pregnancy has been associated with alterations in cortisol levels; however, limited research has assessed cortisol reactivity during pregnancy. Finally, no studies have yet examined whether cortisol reactivity predicts later depressive symptoms during a population-level stressor, such as the COVID-19 pandemic.
Methods:
The current study examined whether cortisol reactivity in perinatal and nulliparous women a year before the onset of COVID-19 predicted increases in depressive symptoms during the initial stage of the pandemic. Participants were 68 women (33 pregnant, Mage = 30.6; 35 nulliparous, Mage = 28.4) who, approximately a year before COVID-19, responded to a depressive symptoms questionnaire and completed a psychosocial stress test, during which they provided salivary cortisol samples. Shortly after the onset of pandemic-related closures (April 2020; postpartum for previously pregnant participants), participants completed follow-up questionnaires assessing current depressive symptoms.
Results:
Analyses showed that cortisol reactivity at baseline predicted increases in depressive symptoms at follow-up. Perinatal and nulliparous women did not differ in this association.
Limitations:
The present study was limited by a moderate sample size and heterogeneity in terms of gestational week, restricting inferences about specific stages of pregnancy.
Conclusions:
Our findings suggest that cortisol reactivity to a laboratory stressor is a biomarker of risk for increased depressive symptoms during ecological stress in women. Biomarkers like these increase our understanding of depression risk and may help to identify individuals in need of interventions.
... It is of course possible, that other confounding factors play a role in this relationship between blunted reactivity and depressive symptoms: next to the above-mentioned individual factors such as experience of childhood adversity (85), obesity and poor cognitive functioning (23), motivation (86), hours of sleep/sleep quality (87), and preference of "eveningness" may be associated with a blunted cardiovascular response (88). Alternatively, a true association between depressive symptoms and blunted HR reactivity is possible and has been reported in healthy populations before [e.g., (89, 90)], also for other measures: for instance, cortisol reactivity to a naturalistic stressor was abolished in those with high depressive symptoms (91). ...
Background
Chronic stress and depressive symptoms have both been linked to increased heart rate (HR) and reduced HR variability. However, up to date, it is not clear whether chronic stress, the mechanisms intrinsic to depression or a combination of both cause these alterations. Subclinical cases may help to answer these questions. In a healthy working population, we aimed to investigate whether the effect of chronic stress on HR circadian rhythm depends on the presence of depressive symptoms and whether chronic stress and depressive symptoms have differential effects on HR reactivity to an acute stressor.
Methods
1,002 individuals of the SWEET study completed baseline questionnaires, including psychological information, and 5 days of electrocardiogram (ECG) measurements. Complete datasets were available for 516 individuals. In addition, a subset (n = 194) of these participants completed a stress task on a mobile device. Participants were grouped according to their scores for the Depression Anxiety Stress Scale (DASS) and Perceived Stress Scale (PSS). We explored the resulting groups for differences in HR circadian rhythm and stress reactivity using linear mixed effect models. Additionally, we explored the effect of stress and depressive symptoms on night-time HR variability [root mean square of successive differences (RMSSD)].
Results
High and extreme stress alone did not alter HR circadian rhythm, apart from a limited increase in basal HR. Yet, if depressive symptoms were present, extreme chronic stress levels did lead to a blunted circadian rhythm and a lower basal HR. Furthermore, blunted stress reactivity was associated with depressive symptoms, but not chronic stress. Night-time RMSSD data was not influenced by chronic stress, depressive symptoms or their interaction.
Conclusion
The combination of stress and depressive symptoms, but not chronic stress by itself leads to a blunted HR circadian rhythm. Furthermore, blunted HR reactivity is associated with depressive symptoms and not chronic stress.
... depression and post-traumatic stress disorder, PTSD) (Pariante and Lightman 2008;Daskalakis et al. 2016). Many studies encompassing rodent and human subjects exposed to ELS or chronic stress have reported a blunted HPA axis response (Albeck et al. 1997;Heim et al. 2001;Burke et al. 2005;Cohen et al. 2006;Carpenter et al. 2007;Tomiyama, Dallman, and Epel 2011;Ouellet-Morin et al. 2011;Grimm et al. 2014;Carroll et al. 2017;Bunea, Szentágotai-Tătar, and Miu 2017;Lam et al. 2019;Xin et al. 2020). Also, exogenous treatment with GC or GR agonist have been shown to result in blunting of the endogenous stress response (Felszeghy, Bagdy, and Nyakas 2000;Kinlein, Wilson, and Karatsoreos 2015), indicating effects on GC negative feedback. ...
Organisms respond to stressors through a coordinated set of physiological and behavioural responses. Zebrafish provides an opportunity to study conserved mechanisms underlying the stress-response that is regulated largely by the neuroendocrine Hypothalamus-Pituitary-Adrenal/Interrenal (HPA) axis, with glucocorticoids (GC) as the final effector. In this study, we evaluated the effect of chronically active GC signalling in early life on the baseline and stress evoked GC(cortisol) levels in larval zebrafish. To this end, we employed an optogenetic actuator, Beggiatoa photoactivated adenylyl cyclase, expressed in the interrenal cells of zebrafish and demonstrate that its chronic activation leads to hypercortisolaemia and dampens the acute-stress evoked cortisol levels, across a variety of stressor modalities during early life. This blunting of stress-response, a phenotype reported by many studies to be observed in human subjects exposed to early-life trauma, was conserved in ontogeny at a later developmental stage. Furthermore, we observe a strong reduction of proopiomelanocortin (POMC)-expressing cells in the pituitary as well as global upregulation of FKBP5 gene expression, impinging on the negative feedback regulation elicited by elevated cortisol levels. Going forward, we propose that this model can be leveraged to tease apart the mechanisms underlying developmental programming of HPA axis by early-life stress and its implications for vulnerability and resilience to stress in adulthood.
... This suggests that a deficit in rACC GABA may reflect impaired inhibition, which may be associated with deficient top-down control and aberrant salience mapping. Similar to prior findings in females with MDD [61], we observed a blunted cortisol response to stress in MDD. This finding may also be related to the number of depressive episodes or young age of the females, given that we previously reported differences in negative stress circuitry responses and hormonal physiology dependent on the age of females with MDD [2,11]. ...
The interplay between cortical and limbic regions in stress circuitry calls for a neural systems approach to investigations of acute stress responses in major depressive disorder (MDD). Advances in multimodal imaging allow inferences between regional neurotransmitter function and activation in circuits linked to MDD, which could inform treatment development. The current study investigated the role of the inhibitory neurotransmitter GABA in stress circuitry in females with current and remitted MDD. Multimodal imaging data were analyzed from 49 young female adults across three groups (current MDD, remitted MDD (rMDD), and healthy controls). GABA was assessed at baseline using magnetic resonance spectroscopy, and functional MRI data were collected before, during, and after an acute stressor and analyzed using a network modeling approach. The MDD group showed an overall lower cortisol response than the rMDD group and lower rostral anterior cingulate cortex (ACC) GABA than healthy controls. Across groups, stress decreased activation in the frontoparietal network (FPN) but increased activation in the default mode network (DMN) and a network encompassing the ventromedial prefrontal cortex–striatum–anterior cingulate cortex (vmPFC–Str–ACC). Relative to controls, the MDD and rMDD groups were characterized by decreased FPN and salience network (SN) activation overall. Rostral ACC GABA was positively associated with connectivity between an overlapping limbic network (Temporal–Insula–Amygdala) and two other circuits (FPN and DMN). Collectively, these findings indicate that reduced GABA in females with MDD was associated with connectivity differences within and across key networks implicated in depression. GABAergic treatments for MDD might alleviate stress circuitry abnormalities in females.
... HPA-axis, Burke, Fernald, Gertler, & Adler, 2005 ; amygdala responsivity, Kim et al., 2013) and as such specific system changes have been proposed as biological mediators that link early life economic hardships to later life adverse outcomes. However, given the biological interactions between all the systems that work together to achieve body homeostasis, no one pathway is solely responsible for how material hardship gets "underneath the skin", and more than likely all systems contribute to the allostatic load "weathering" effects on development (Geronimus, Hicken, Keene, & Bound, 2006). ...
Experiencing poverty during childhood may prompt experience-dependent neural adaptations. These manifest through functional connectivity patterns across networks thought to support cognitive and socio-emotional processing. Interrelated network connectivity disruptions have been associated with the development of internalizing disorders. Connectome-wide network characterizations of functional connectivity in adolescents who grew up in poverty are lacking. To this end, this dissertation aimed to characterize the association between family material hardship, connectome-wide network connectivity and internalizing symptoms in adolescence. The introductory chapter proposes material hardship, which directly measures a family's experiences with unmet basic needs (e.g., no access to food) as a better alternative to income-based measures used in research. Subsequently, in Chapters Two and Three, network contingency analyses were conducted to characterize connectome-wide connectivity associated with lifetime family material hardship for adolescents drawn from a national longitudinal study. Correlational analyses evaluating the association between network connectivity and current adolescent internalizing symptoms were done. Notably, the mixed findings across the two studies suggest that connectome-wide adaptations confer both cost and benefits to youth who experienced material hardship. Data suggests that altered network connectivity may be protective and that not everyone who experiences material hardship develops internalizing symptoms. In the final chapter, the limitations and implications of the present findings are discussed. Recommendations for more multi-method research to better characterize the association between brain function and poverty are made.
... However, the meta-analysis of Burke et al. [31] suggested that stress reactivity might depend on depression severity since participants with more severe depressive symptoms tended to show a reduced cortisol response (flat and unresponsive pattern of cortisol secretion) in response to laboratory stress. The notion of a blunted cortisol reactivity is in line with other experimental and naturalistic studies [32][33][34][35][36]. In summary, previous research suggests that the cortisol reactivity of people with depressive disorders may differ from healthy individuals, however these differences seem to depend on several extraneous factors. ...
Physical activity is associated with a favourable (blunted) cortisol stress reactivity in healthy people. However, evidence from experimental study and with psychiatric patients is missing. This study examines whether exercise training impacts on cortisol stress reactivity in inpatients with major depressive disorder (MDD). These new insights are important because the stress reactivity of healthy people and patients with severe symptoms of depression might differ. Methods: The study was designed as a randomized controlled trial (trial registration number: NCT02679053). In total, 25 patients (13 women, 12 men, mean age: 38.1 12.0 years) completed a laboratory stressor task before and after a six-week intervention period. Nine samples of salivary free cortisol were taken before and after the Trier social stress test (TSST). Fourteen participants took part in six weeks of aerobic exercise training, while 11 patients were allocated to the control condition. While the primary outcome of the study was depressive symptom severity, the focus of this paper is on one of the secondary outcomes (cortisol reactivity during the TSST). The impact of aerobic exercise training was examined with a repeated-measures analysis of variance. We also examined the association between change in depression and cortisol response via correlational analysis. Cortisol reactivity did not change from baseline to post-intervention, either in the intervention or the control group. Participation in six weeks of aerobic exercise training was not associated with participants’ cortisol reactivity. Moreover, depressive symptom change was not associated with change in cortisol response. Aerobic exercise training was not associated with patients’ stress reactivity in this study. Because many patients initially showed a relatively flat/blunted cortisol response curve, efforts might be needed to find out which treatments are most efficient to promote a normalization of HPA axis reactivity.
... In PTSD studies, some researchers have found that stress can trigger greater cortisol reactivity in anticipation of a stressor in PTSD patients (8,9). In MDD studies, researchers have found that the HPA responses to acute stress in MDD was similar to controls (10) or relatively blunted (11,12). In the recent decade, blunted cortisol response was found in adolescents with moderate or severe depression (13) and soldiers who showed greater increase in PTSD symptomatology (14). ...
The hypothalamic-pituitary-adrenocortical (HPA) function is crucial for adaptation to stress and recovery of homeostasis. Physiological alteration in the HPA axis has been shown to play a pivotal role in the generation of stress-related disorders. A growing number of studies have begun to identify which variables are possible to predict individual HPA response and associated stress vulnerability. The current study investigated the relationship between working memory and the subsequent magnitude of HPA response to psychosocial stress in a non-clinical population. Working memory was assessed utilizing an n-back task (2/3-back) in thirty-nine healthy young men, whose electroencephalograms were recorded. The HPA response was measured using the percentage increase in cortisol to an acute psychosocial stress protocol called the Trier Social Stress Test (TSST). Our results show that longer reaction time and smaller amplitude of P2 predict a relatively lower HPA response to stress. Our study provides new insights into how neurocognitive factors can be used to predict HPA response to acute stress.
... Importantly, the offspring also showed blunted stress responses (Rodgers et al., 2013). These results are unsurprising as dysregulation of brain's stress circuitry is a common feature across psychiatric diseases, with studies reporting both hyper-and hypoactivity of the hypothalamic-pituitary-adrenal stress axis (Bale & Epperson, 2015;Burke, Fernald, Gertler, & Adler, 2005;Martin, Ressler, Binder, & Nemeroff, 2010). These data suggest that ncRNA expression is altered in offspring following paternal stress later in life; however, these changes do not produce detectible behavioral differences in offspring. ...
Depression and anxiety risk are highly influenced by both genetic and environmental factors. Recently, it has been proposed that epigenetic mechanisms may also contribute to the transmission of both depression‐ and anxiety‐related behaviors across multiple generations. This review highlights long‐lasting epigenetic alterations observed in offspring of fathers, including some distinct effects on male and female offspring, in animal models. Available evidence emphasizes how both the developmental time point and the type of paternal stress (social vs asocial) influence the complex transmission patterns of these phenotypes to future generations. This research is critical in understanding the factors that influence risk for depression and anxiety disorders and has the potential to contribute to the development of innovative treatments that can more precisely target vulnerable populations.
... Altered HPA axis function is common in MDD (Burke et al. 2005, Lupien et al. 2009), and the onset of depressive episodes is often attributed to stressful life events (Jessen et al. 2014, Kendler et al. 2000. The association of stress with MDD supports a stressexposure model of MDD in which depressive episodes are triggered by stressful events and maladaptive responding (Hankin et al. 2007, Liu & Alloy 2010. ...
This article reviews the interactions of estrogen changes and psychosocial stress in contributing to vulnerability to major depressive disorder (MDD) in women. Estrogen modulates brain networks and processes related to changes in stress response, cognition, and emotional dysregulation that are core characteristics of MDD. Synergistic effects of estrogen on cognitive and emotional function, particularly during psychosocial stress, may underlie the association of ovarian hormone fluctuation and depression in women. We propose a model of estrogen effects on multiple brain systems that interface with stress-related emotional and cognitive processes implicated in MDD and discuss possible mechanisms through which reproductive events and changes in estrogen may contribute to MDD risk in women with other concurrent risk factors. Expected final online publication date for the Annual Review of Clinical Psychology Volume 15 is May 7, 2019. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
... Two separate lines of research can inform our understanding of why depressive symptoms, in some cases, predict a lower cortisol and higher DHEA (i.e. a lower cortisol/DHEA ratio). First, scholars have found that depressive symptoms are associated with a blunted cortisol response to a stressor (Burke et al. 2005), as well as a dampened cortisol awakening response and diurnal rhythm (Doane et al. 2013;Stetler and Miller 2005). Second, researchers have found higher DHEA concentrations among patients diagnosed with major depressive disorder (Assies et al. 2004), as well as healthy individuals reporting higher levels of depressive symptoms (Morrison et al. 2001). ...
Objective:
Racial discrimination (RD) is hypothesized to dysregulate the production of stress reactive hormones among African Americans. Psychological processes that may mediate the association between RD and such dysregulation (e.g. cortisol/DHEA ratio) are not well articulated. Organizational religious involvement (ORI) has been discussed as a psychological protective factor within the context of RD, but our understanding of ORI as a physiological protective factor remains limited. We evaluated whether RD was directly and indirectly (through depressive symptoms) associated with an imbalance of cortisol and DHEA hormones, and whether ORI buffered these direct and/or indirect pathways.
Design:
Data were drawn from the Flint Adolescent Study, an ongoing interview study of youth that began in 1994. Participants were 188 African American emerging adults (47.3% Female, ages 20-22). We used mediation and moderated-mediation analyses, as outlined by Hayes [2012. PROCESS SPSS Macro. [Computer Software and Manual]. http://www.afhayes.com/public/process.pdf ], to evaluate the study aims.
Results:
We found that depressive symptoms mediated the association between RD and the cortisol/DHEA ratio. We also found that depressive symptoms mediated the association between RD and the cortisol/DHEA ratio for individuals reporting low and moderate levels of ORI, but not at high levels.
Conclusions:
Our findings support the socio-psychobiological model of racism and health [Chae et al. 2011 . "Conceptualizing Racial Disparities in Health: Advancement of a Socio-Psychobiological Approach." Du Bois Review: Social Science Research on Race 8 (1): 63-77. doi: 10.1017/S1742058X11000166 ] and suggest that the psychological toll of RD can confer physiological consequences. Moreover, ORI may disrupt pathways from RD to cortisol/DHEA ratio by buffering the psychological toll of RD.
... An acute stressor may have even more pronounced consequences for parent outcomes in disadvantage contexts, where caregivers are exposed to more frequent and pervasive stressors of poverty, community violence, domestic violence, and disorganized neighborhoods. Naturalistic and laboratory studies have revealed that persistent exposure to environmental stressors, along with high levels of depression or anxiety, are related not only to higher levels of cortisol and perceived stress, but also to differences in stress reactivity and impaired recovery following an acute stressor (Burke, Davis, Otte, & Mohr, 2005;Burke, Fernald, Gertler, & Adler, 2005;Hubert & de Jong-Meyer, 1992;van Eck, Berkhof, Nicolson, & Sulon, 1996). Consequently, it is likely that a violent or stressful event may tax caregivers' capabilities even further in more disadvantaged and unstable contexts, capturing their attention, depleting their self-control (Lynch & Cicchetti, 2002), and eventually compromising their skills and engagement when they are most needed. ...
... It has been shown that high HPA axis activity and serum cortisol level is accompanied with depression (9,49). Several studies have also revealed that depression is associated with higher baseline cortisol levels, blunted stress reactivity, and impaired recovery from psychological stress (50,51). Moreover, marked activation of the HPA axis has been reported in the depressed patients that can be normalized by antidepressant therapy (52,53). ...
Objective(s)
Chronic stress has been linked to the pathophysiology of mood disorders including anxiety and depression. In this study, we aimed to investigate the effect of troxerutin (TRX), as a flavonol, on stress-induced anxiety and depression.
Materials and Methods
56 animals were randomly divided into seven groups (n=8 per group) as follows: control, saline, TRX 50, TRX 150, TRX 300, Diazepam, and Imipramine. Chronic mild stress (CMS) was induced by restraining animals in Plexiglas cylinders for 1 hr each day for 25 consecutive days. Different doses (50, 150, and 300 mg/kg, oral gavage) of troxerutin was gavaged for 14 consecutive days. At the end of treatments, anxiety- and depressive-like behaviors were tested using elevated plus-maze (EPM), open field test (OFT), and forced swimming test (FST).
Results
CMS significantly increased immobility (P<0.05) and decreased swimming (P<0.01) time in FST. However, different doses of troxerutin significantly decreased immobility (P<0.01) and increased swimming (P<0.001) time. CMS also significantly (P<0.01) decreased the percentage of open arm entrance (%OAE), whereas troxerutin significantly increased both %OAE and percentage of open arm time (%OAT) in the EPM. Moreover, CMS significantly decreased time spent in the center (P<0.001) and the number of center entrances (P<0.01) in the OFT. However, troxerutin significantly increased time spent in the center and number of the entrances crossing. Furthermore, CMS significantly increased serum cortisol levels and troxerutin decreased it.
Conclusion
Troxerutin demonstrated anxiolytic- and antidepressant-like activities in rodents, which supports the use of herbal medicine in the mood disorders.
... Two neurobiological foci of the stress response are the hypothalamic-pituitary-adrenal axis (HPA), and the neuroimmune system. Individuals with depression have HPA dysregulation reflected in higher basal cortisol which can be associated with blunted response to stress, exaggerated HPA responses during recovery from stress, and altered responses to dexamethasone (Belvederi Murri et al., 2014;Burke et al., 2005a;Burke et al., 2005b;Lopez-Duran et al., 2009;Morris et al., 2012). Results vary across studies with factors such as age and time of blood collection. ...
Patients with depression and rodent models of depression show increased cytokines and activated microglia. Fawn Hooded (FH/Wjd) rats have long been used as a model of depression based on their depressive-like behaviors, high basal corticosterone levels and altered serotonergic levels, but little is known about the neuroimmune function in this model. To test whether depressive-like behaviors relate to dysfunction of the neuroimmune system, depressive-like behaviors in the forced swim test (FST) and corticosterone (CORT) response to the swim test were compared in male Fawn Hooded versus Wistar rats, and cytokine levels in plasma and brain and plasma CORT in response to lipopolysaccharide (LPS, an endotoxin that activates the neuroimmune system) or 1 h restraint were measured. Fawn Hooded rats had more depressive-like behaviors in the FST (decreased swim time and increased immobility) and increased overall plasma CORT compared with Wistar rats. Additionally, Fawn Hooded rats exhibited blunted brain and plasma cytokine response to LPS compared with Wistar rats, an effect that might be related to the blunted plasma CORT response to LPS. No strain differences were found on these measures in response to restraint stress. These results suggest that Fawn Hooded rats have a depressive-like phenotype potentially more closely associated with serotonin dysregulation and a dysregulated HPA axis and remain a relevant model for further defining the role of these systems in depressive conditions.
https://authors.elsevier.com/c/1XKjkbfPj1FFH
... Depression is common among mothers, and is a major source of disability [1,2], particularly among the poor [3]. In a study of mothers in rural Mexico, 51% were identified as having high depressive symptoms, above the US cutoff for depression [4]; similarly, a study in low-income areas of urban Mexico found that 60% of women had depressive symptoms above the US cutoff [5]. Maternal depression has been identified as a key risk factor for poor child development [6]. ...
Over 50% of mothers in rural Mexico have high depressive symptoms, and their children's health and development are likely to be negatively affected. A critical question is whether children vary in their vulnerability to the effects of high maternal depressive symptoms according to their indigenous ethnicity, maternal education, or household wealth. Our sample included 4442 mothers and 5503 children from an evaluation of Mexico's social welfare program. Maternal depressive symptoms were assessed using the Center for Epidemiologic Studies Depression (CES-D) Scale, and child behavior was measured using an adapted version of the Behavior Problems Index (BPI). Multiple linear regression models were used to explore the associations between maternal depressive symptoms and child behavior problems, and the heterogeneity of associations by indigenous ethnicity, maternal education, and household assets. We found that having greater maternal depressive symptoms was significantly associated with having a child with more behavior problems (β = 0.114, p < 0.0001, [95% CI 0.101, 0.127]), in adjusted models. In tests of heterogeneity, the association between maternal depressive symptoms and child behavior problems was strongest in households with indigenous ethnicity, low maternal education, or in households with fewer assets. These results strengthen the case for effective mental health interventions in low- and middle-income countries, particularly among the most vulnerable families where mothers and children appear to be at the greatest risk.
... Also, studies of the effects of minor daily stressors have found that, after a certain point, additional stressors do not worsen mood, with the exception of interpersonal conflicts (Bolger, DeLongis, Kessler, & Schilling, 1989). Physiologically, depression, in particular, is associated with a blunted rather than hyperresponsive HPA axis response to repeated stress (Burke, Fernald, Gertler, & Adler, 2005;Miller, Chen, & Zhou, 2007). ...
Objective:
To test whether effects of multiple (up to 5) disasters on mental health responses were cumulative (additive effects), or whether an earlier disaster produced sensitization (higher) or habituation (lower) responses to a later one.
Method:
The Gulf Resilience on Women's Health study interviewed 1,366 southern Louisiana women regarding their exposure to Hurricanes Katrina, Rita, Gustav, and Ike and the Gulf oil spill (measured several ways), and administered validated measures of symptoms of depression and posttraumatic stress disorder (PTSD). Multiple linear and logistic regression with disaster exposures entered singly, combined, and as an interaction were used to model mental health.
Results:
Both exposure to the oil spill and hurricane disaster were associated with likely depression and PTSD, consistent with a cumulative model, but we did not find statistical interactions that would suggest sensitization or habituation. When results were examined with continuous symptom measures of depression and PTSD, they were similar, with the exception that exposure to the oil spill and experiencing illness or injury because of the hurricane disaster showed a significant interaction (p < .05) in a manner consistent with a sensitization effect when predicting PTSD symptoms. The results of this study point mainly to a cumulative risk for the mental health effects of multiple disasters, although some indication of sensitization occurred among those with particularly severe experiences. There was no evidence for habituation.
Conclusions:
These findings may guide efforts to assist those in regions experiencing multiple disasters that occur in close sequence. (PsycINFO Database Record
... Interestingly, these relationships were inverted relative to each other, such that physical activity was a positive predictor of AUC g and a negative predictor of AUC i , suggesting an overall greater magnitude of cortisol output, yet a blunted cortisol response in those individuals who are more active. Since depressive patients have been shown to have blunted responses (i.e., lowered AUC i ) relative to healthy controls [62,63], this finding may indicate that physical activity was beneficial in moving the CAR to a more healthy profile. ...
Background:
The cortisol awakening response (CAR) has been used as a biomarker of stress response in a multitude of psychological investigations. While a myriad of biochemical responses have been proposed to monitor responses to exercise training, the use of CAR within the exercise and sports sciences is currently limited and is a potentially underutilized variable. Therefore, the purpose of this review was to collate studies that incorporate both exercise and CAR, in an effort to better understand (a) whether CAR is a useful marker for monitoring exercise stress and (b) how CAR may be most appropriately used in future research.
Methods:
A systematic review of the literature was conducted, following PRISMA guidelines. Searches were conducted using PubMed, SportDISCUS, Scopus, and PsychInfo databases, using search terms related toCAR and exercise and physical activity.
Results:
10,292 articles were identified in the initial search, with 32 studies included in the final analysis. No studies investigated the effects of laboratory-controlled exercise on CAR. Variable effects were observed, possibly due to inconsistencies in study design, methodology, population, and CAR analysis. The available literature suggests a threshold of exercise may be required to alter the HPA axis and affect CAR. Moreover, CAR may represent a combination of previous exercise load and upcoming stress, making current interpretation of field-based observational research challenging.
Conclusions:
More research is needed to fully elucidate the influence of exercise on CAR and address a number of gaps in the literature, including controlling exercise load, consistent sample collection, and CAR calculation and analysis.
... Also, studies of the effects of minor daily stressors have found that, after a certain point, additional stressors do not worsen mood, with the exception of interpersonal conflicts (Bolger, DeLongis, Kessler, & Schilling, 1989). Physiologically, depression, in particular, is associated with a blunted rather than hyperresponsive HPA axis response to repeated stress (Burke, Fernald, Gertler, & Adler, 2005;Miller, Chen, & Zhou, 2007). ...
... Additionally, circadian-mediated cortisol levels that is the effect of the time of day play important roles in stress reaction 19 and cognition 20 . The varying influence of cortisol on memory due to the time of day relative to diurnal flux is connected to the relative occupancy of mineralocorticoid or glucocorticoid receptor subtypes (MR and GR subtypes, respectively), which have different affinities for glucocorticoids 21 . ...
Few studies have investigated the relationship between cortisol diurnal rhythm and cognitive function in healthy young adults, especially for emotional memory. To address this deficiency, this study examined the effect of diurnal cortisol slope (DCS) and heart rate variability (HRV) on emotional memory. Participants included healthy volunteers (44 men and 23 women; mean age 20.60 yrs). Participants were shown emotionally arousing slides and were asked to return to the laboratory one week later where they were given a “surprise” memory test to examine their emotional memory retention. Participants were asked to collect saliva samples at four time points (08:00, 11:00, 15:00, and 20:00) on the experimental days; these samples were used to calculate the DCS. Moreover, HRV was measured during the experiment. The multiple linear regression analysis revealed that declarative memory ability, sleep duration, and the DCS were the final significant determinants for emotional memory enhancement (B = −20.41, 0.05, −48.20, ps < 0.05), with participants having flatter cortisol slopes showing reduced or absent emotional memory enhancement. These findings are discussed in reference to the possible effects of diurnal rhythm mechanisms of the hypothalamus-pituitary-adrenal axis and the autonomic nervous system on emotional memory.
... La fatiga, los síntomas depresivos y las alteraciones del sueño han mostrado relación con estos índices de cortisol Burke, Fernald, Gertler y Adler, 2005;Ahrens et al., 2008;Backhaus, Junghanns y Hohagen, 2004;Ho, Fong, Chan y Chan, 2013). Debido a que los síntomas de fatiga, depresión y alteraciones de sueño ocurren en conjunto en los pacientes con cáncer e interaccionan con la respuesta del cortisol al despertar (CAR) el objetivo de este estudio es examinar la relación entre la fatiga, la depresión, la calidad de sueño e índices de cortisol, así como comparar si existen diferencias entre el estadio de la enfermedad en cuanto a estas mismas variables. ...
The aim of this study was to evaluate the relationship between fatigue, depressive symptomatology, sleep quality and cortisol measurement and identify variables that explain the fatigue in women with breast cancer. Seventeen women with breast cancer were evaluated prior to chemotherapy treatment, they provided 12 samples of saliva during two consecutive days and answered the scales of fatigue (MFI), depression (BDI) and sleep quality (PSQI). The results show that sleep latency explains 41.7 % of the reduction of activity and daytime dysfunction explains 48.8 % of mental fatigue, which suggests an approach to intervention at this stage of the cancer process.
... While both groups had PTSD symptoms, cortisol levels moved in different directions after trauma-activation suggesting that when depressive symptoms are comorbid with PTSD, the depressive HPA and cortisol mechanisms predominate over the PTSD mechanisms. Blunt cortisol associated with depressive symptoms may relate to mechanisms of psychological disengagement with environmental stressors (Burke et al., 2005) and excessive shutting down of the hypothalamic-pituitary-adrenal cortical (HPA) axis due to impairment in negative feedback. An enhanced cortisol response in PTSD alone may be related with reexperiencing symptoms (Dekel et al., 2013a). ...
Background: Although depression symptoms are often experienced by individuals who develop posttraumatic stress disorder (PTSD) following trauma exposure, little is know about the biological correlates associated with PTSD and depression co-morbidity vs. those associated with PTSD symptoms alone.
Methods: Here we examined salivary cortisol responses to trauma activation in a sample of 60 survivors of the World Trade Center attacks on September 11, 2001. Participants recalled the escape from the attacks 7 months post 9/11. Salivary cortisol levels were measured before and after their recollection of the trauma. PTSD, depression, and somatic symptoms were also assessed. From the behavioral assessment scales, the participants were grouped into three conditions: those with comorbid PTSD and depressive symptoms, PTSD alone symptoms, or no-pathology.
Results: Baseline and cortisol response levels differed between the comorbid, PTSD alone, and no-pathology groups. Individuals endorsing co-morbid symptoms had higher PTSD and somatic symptom severity and their cortisol response decreased following their trauma reminder while a trend of an elevated response to the trauma was found in the PTSD alone group. Our findings show distinct psychological and biological correlates related to the endorsement of PTSD with and without depression comorbidity.
Conclusions: The findings suggest that comorbidity symptoms manifestation entails a separate trauma induced condition from PTSD. Future research on biological correlates of comorbid PTSD and depression is warranted.
... and a significant condition by group interaction effect (p = .03). sol response to stress in association with depressive symptoms (Burke et al., 2005b;Peeters et al., 2003). Heim et al. (2000a,b) reported that a higher cortisol response to stress only in MDD patients with childhood trauma, which was not replicated in our study. ...
Background:
Adverse childhood experiences (ACE) increase the risk to develop major depressive disorder (MDD) and obesity or metabolic syndrome in adulthood. In addition, ACE may be associated with an exaggerated endocrine response to stress, which, in turn, may lead to enhanced food intake resulting in obesity and metabolic problems.
Methods:
We systematically examined the stress response and consecutive food intake in 32 women with MDD and ACE as determined by a clinical interview (Early Trauma Inventory), 52 women with MDD without ACE, 22 women with ACE but no current or lifetime MDD and 37 healthy women without either MDD or ACE. All participants underwent a psychosocial stress test (Trier Social Stress Test, TSST) and a control condition (Placebo-TSST) before they were offered a buffet of snacks. Participants were not aware that the primary outcome variable was the amount of consumed kilocalories (kcal).
Results:
The four groups did not differ in demographic variables. Stress resulted in higher cortisol release and higher blood pressure compared to the control condition. Patients with MDD without ACE had a significantly lower cortisol response to stress compared to controls. Across groups, we found higher kcal intake after stress compared to the control condition. Comparing high and low cortisol responders to stress, higher kcal intake after stress was only seen in those with low cortisol release.
Conclusions:
This study provides evidence that blunted rather than enhanced cortisol release to stress might lead to increased food intake, independent from MDD and ACE.
... delayed recovery of cortisol levels after exposure to a stressor are both thought to be indications of hypocortisolism, a form of stress-system dysregulation (Adam, Klimes-Dougan, & Gunnar, 2007;Burke, Davis, Otte, & Mohr, 2005;Burke, Fernald, Gertler, & Adler, 2005;Heim, Ehlert, & Hellhammer, 2000;van Goozen et al., 1998). ...
Objective:
Race/ethnicity and socioeconomic status are both associated with stress physiology as indexed by cortisol. The present study tested the extent to which racial/ethnic disparities in cortisol reactivity are explained by socioeconomic status.
Method:
The sample consisted of 296 racially and socioeconomically diverse children ages 8-11 (47% boys). Mothers reported on children's stressors and socioeconomic status; salivary cortisol levels were assessed before and after the Trier Social Stress Test.
Results:
Results demonstrated that racial group differences in cortisol reactivity were partially accounted for by differences in socioeconomic status, but racial group differences in cortisol recovery were not.
Conclusions:
These findings suggest that cumulative effects of stress and disadvantage may result in differences in stress response physiology as early as middle childhood, and that race-specific mechanisms account for additional variance in cortisol reactivity and recovery. (PsycINFO Database Record
... Indeed, decreased cortisol and catecholamine metabolite responses to a mental stressor were risk factors for the development of vascular diseases in a Black African cohort exhibiting symptoms of depression [24]. There still remains no clear cut or generally accepted model for cortisol responses in depression, as both blunted and increased cortisol activities have previously been noted [21,25]. Blunted cortisol responses were apparent in individuals with depressive symptoms after exposure to the Stroop test [13]. ...
Sympathetic system hyperactivity and depression are related to cardiac remodelling in Black men. We investigated whether sympathetic system hyperactivity and depressive symptoms are related to retinal vascular dysregulation. A total of 76 Black and 83 White men (23–68 years of age) from the SABPA study were included. Depressive symptoms, 24h pulse pressure (PP), fasting blood and 24-hour urinary catecholamine data were obtained. Retinal vascular calibre was quantified from digital photographs using standardized protocols. Black men demonstrated increased (p < 0.05) hyperpulsatile pressure (PP > 50 mmHg), hypertension (78.9 % vs 48.4%) and depression (34.2% vs. 13.3%) prevalence compared to White men. Despite lower epinephrine levels, epinephrine was associated with arteriolar narrowing and venular widening in the Black men [Adj R2 −0.37 (95% CI: −0.66, −0.09), p=0.013; Adj R2 0.35 (95% CI: 0.13, 0.57), p=0.003]. This might suggest ß-adrenergic hyporesponsivity to epinephrine, which was accompanied by hyperpulsatile blood pressure in the Black group. In the White group, depressive symptoms and norepinephrine were associated with retinal arteriolar narrowing. A profile of ß-adrenergic hyporesponsivity, indicative of a chronically challenged sympathetic system, was associated with retinal vascular remodelling in Black men. ß-adrenergic hyporesponsivity as a result of chronic stress emphasized central control of the brain on the circulatory system irrespective of the vascular bed.
... If the stressor is prolonged, repeated or uncontrollable the physiological stress response may become inadequate, and ultimately, result in adverse health problems [34,35]. For example, stress-induced cortisol dysregulation has been positively associated clinical depression [36,37], cardiovascular disease [38,39], type 2 diabetes and stroke [34], and dysregulation of the sympatho-adrenal medullary system has been positively associated with asthma [40] and atherosclerosis [41]. Therefore, it is important to establish whether the sympathoadrenal medullary system and/or the hypothalamo-pituitary adrenal axis are affected when working on-call from home. ...
On-call work is becoming an increasingly common work pattern, yet the human impacts of this type of work are not well established. Given the likelihood of calls to occur outside regular work hours, it is important to consider the potential impact of working on-call on stress physiology and sleep. The aims of this review were to collate and evaluate evidence on the effects of working on-call from home on stress physiology and sleep. A systematic search of Ebsco Host, Embase, Web of Science, Scopus and ScienceDirect was conducted. Search terms included: _on-call_, _on call_, _standby, sleep_, _cortisol, heart rate_, _adrenaline_, _noradrenaline_, _nor-adrenaline_, _epinephrine_, _norepinephrine_, _nor-epinephrine_, _salivary alpha amylase_ and _alpha amylase_. Eight studies met the inclusion criteria, with only one study investigating the effect of working on-call from home on stress physiology. All eight studies investigated the effect of working on-call from home on sleep. Working on-call from home appears to adversely affect sleep quantity, and in most cases, sleep quality. However, studies did not differentiate between night’s on-call from home with and without calls. Data examining the effect of working on-call from home on stress physiology were not sufficient to draw meaningful conclusions.
... women (16%) as it is for men (9%) (Slone et al., 2006). Another study in urban Mexico found high depressive symptoms in 60% of poor women (Burke et al., 2005). Lower education and having experienced childhood trauma are also associated with higher risk for depressive disorders among Mexicans (Slone et al., 2006). ...
Objective: We examine whether having depressive symptoms (DS) is associated with different responses to cigarette package health warning labels (HWLs) before and after the implementation of pictorial HWLs in Mexico. Method: We analyze data from adult smokers from Wave 4 and Wave 5 (n = 1,340) of the International Tobacco Control Policy Evaluation Project in Mexico. Seven Center for Epidemiological Studies Depression Scale (CES-D) items assessed DS, with scores ≥7 indicating elevated DS. Outcomes included: attention to HWLs, cognitive responses to HWLs, tobacco constituents awareness, putting off smoking due to HWLs, avoidance of HWLs, and awareness of telephone support for cessation (i.e., quitlines). Mixed effects models were used to assess main and interactive effects of DS and time (i.e., survey wave) on each outcome. Results: All HWL responses increased over time, except putting off smoking. Statistically significant interactions were found between DS and time for models of tobacco constituents awareness (b = −0.36, SE = 0.15, p = .022), putting off smoking (OR = 0.41, 95% CI [0.25, 0.66]), avoidance of HWLs (OR = 1.84, 95% CI [1.03, 3.29]), and quitline awareness (OR = 0.35, 95% CI [0.21, 0.56]). Compared to smokers with low DS, smokers with elevated DS reported stronger HWL responses at baseline; however, HWL responses increased over time among smokers with low DS, whereas HWL responses showed little or no change among smokers with elevated DS. Discussion: Population-level increases in HWL responses after pictorial HWLs were introduced in Mexico appeared mostly limited to smokers with low DS. In general, however, smokers with elevated DS reported equivalent or stronger HWL responses than smokers with low DS. (PsycINFO Database Record (c) 2016 APA, all rights reserved)
... It is possible that such studies also included subclinical elevations in depressive mood that might exist among a sample of individuals without clinical depression. In addition, many similar studies have not explicitly excluded asthmatic participants [8,10,73]. It is also possible that our sample with a strong representation of undergraduate students did not feel overly threatened by the task. ...
... Some studies have examined stress and diet quality in adolescents [15] and in high-income working adults [16], but findings are inconsistent. Mixed findings may relate to how stress and depression might interact with diet quality and BMI in different socioeconomic subgroups [26,57]. Socioeconomically disadvantaged populations experience more stress and might be more depressed than advantaged populations. ...
Background
Stress has been associated with poor eating behaviors and diet quality, as well as high body mass index (BMI). Low-income women may be particularly vulnerable to stress and severe obesity. Yet it is unknown how stress increases the risk of severe obesity through disordered eating behaviors and poor diet quality or through mechanisms independent of diet.
Methods
We examined cross-sectional data from women (n = 101) with a child enrolled in the Special Supplemental Nutrition Program for Women, Infants, and Children in Cumberland County, North Carolina (spring 2012). We collected measured heights and weights to calculate BMI. Using structural equation modeling, we differentiated pathways from stress to weight status: (1) indirectly through eating behaviors (cognitive restraint, emotional eating, and uncontrolled eating) and diet quality, which we examined with the Healthy Eating Index 2010 and 24-h dietary recalls, and (2) directly through possible unmeasured risk factors independent of diet. The analysis controlled for race/ethnicity, income, age, whether the dietary recall day was typical, and whether the respondent completed one or two 24-h dietary recalls.
Results
Perceived stress was positively associated with uncontrolled eating (β = 0.38, p < 0.001) and emotional eating (β = 0.50, p < 0.001). However, higher stress was not associated with weight status through eating behaviors and diet quality. Independent of eating behaviors and diet quality, stress was positively associated with severe obesity (β = 0.26, p = 0.007).
Conclusions
Improving stress coping strategies for low-income women may improve eating behaviors and reduce severe obesity.
Electronic supplementary material
The online version of this article (doi:10.1186/s12937-015-0110-4) contains supplementary material, which is available to authorized users.
... Specifically, alterations in cortisol patterns, such as a blunted cortisol response after awakening (i.e., CAR) and lower daily total cortisol output (i.e., area under the curve (AUC)), have been associated with increased risk for MDD (Dedovic et al. 2006). In addition, several studies have found blunted diurnal cortisol patterns (Jarcho et al. 2013;Knight et al. 2010) or a blunted cortisol response to psychological stressors (Burke et al. 2005) among women who suffer from depression. ...
Postpartum depression (PPD) has been associated with a number of negative maternal and infant health outcomes. Despite these adverse health effects, few studies have prospectively examined patterns of pre- and postnatal stress that may increase a woman's risk for PPD. The current study examined whether the timing of altered salivary cortisol patterns and perceived stress levels during pregnancy and at 3 months postpartum was associated with PPD symptoms among 100 low-income mothers. Higher levels of PPD were found among women with a lower cortisol awakening response (first and second trimester), lower average daily cortisol (second trimester), a flatter diurnal cortisol pattern (second and third trimester and at 3 months postpartum), and a less abrupt drop in both cortisol and perceived stress from the third trimester to 3 months postpartum. These results support the need for early screening and regulation of stress levels to promote depression prevention efforts in at-risk populations.
... La fatiga, los síntomas depresivos y las alteraciones del sueño han mostrado relación con estos índices de cortisol Burke, Fernald, Gertler y Adler, 2005;Ahrens et al., 2008;Backhaus, Junghanns y Hohagen, 2004;Ho, Fong, Chan y Chan, 2013). Debido a que los síntomas de fatiga, depresión y alteraciones de sueño ocurren en conjunto en los pacientes con cáncer e interaccionan con la respuesta del cortisol al despertar (CAR) el objetivo de este estudio es examinar la relación entre la fatiga, la depresión, la calidad de sueño e índices de cortisol, así como comparar si existen diferencias entre el estadio de la enfermedad en cuanto a estas mismas variables. ...
El objetivo de este estudio fue evaluar la relación entre la fatiga, la sintomatología de depresión y la calidad de sueño con indicadores de cortisol y determinar cuáles son las variables que explican la fatiga en mujeres con cáncer de mama. Participaron 17 mujeres con cáncer de mama previo al tratamiento de quimioterapia, las cuales proporcionaron 12 muestras de saliva durante dos días consecutivos y respondieron las escalas de Fatiga (MFI), Depresión (BDI) y Calidad de Sueño (ICSP). Los resultados obtenidos muestran que la latencia de sueño explica en un 41.7% la reducción de la actividad y que la disfunción diurna explica en un 48.8% de la fatiga mental, lo que nos sugiere un enfoque de intervención en esta fase del proceso del cáncer.
Early life stress (ELS) exposure alters stress susceptibility in later life and affects vulnerability to stress‐related disorders, but how ELS changes the long‐lasting responsiveness of the stress system is not well understood. Zebrafish provides an opportunity to study conserved mechanisms underlying the development and function of the stress response that is regulated largely by the neuroendocrine hypothalamus–pituitary–adrenal/interrenal (HPA/I) axis, with glucocorticoids (GC) as the final effector. In this study, we established a method to chronically elevate endogenous GC levels during early life in larval zebrafish. To this end, we employed an optogenetic actuator, beggiatoa photoactivated adenylyl cyclase, specifically expressed in the interrenal cells of zebrafish and demonstrate that its chronic activation leads to hypercortisolaemia and dampens the acute‐stress evoked cortisol levels, across a variety of stressor modalities during early life. This blunting of stress–response was conserved in ontogeny at a later developmental stage. Furthermore, we observe a strong reduction of proopiomelanocortin ( pomc )‐expression in the pituitary as well as upregulation of fkbp5 gene expression. Going forward, we propose that this model can be leveraged to tease apart the mechanisms underlying developmental programming of the HPA/I axis by early‐life GC exposure and its implications for vulnerability and resilience to stress in adulthood.
Background
Evidence indicates sex differences in stress response and mental health challenges. Psychobiological research of early symptoms of psychopathology has suggested that cortisol, as a marker of stress, is positively associated with depressive mood and anxiety in adolescents. To date, no study has examined sex differences in the relationships between cortisol levels and negative mood among Moroccan youth.
Methods
A total of 332 Moroccan secondary students (171 female) aged 11 to 20 completed a range of psychological measures and provided two morning saliva samples across atwo-hour period. We hypothesized that females would show greater levels of depression and anxiety symptoms than males. We also anticipated positive relationships between cortisol and those symptoms.
Results and Discussion
The results demonstrated the expected cortisol morning decline due to the diurnal pattern. Higher anxiety (p < .001), higher depressive mood (p < .001), and more clinically relevant depression were found in the females (47.7%) than the males (22.5%; p < .001). In addition, anxiety (p < .05) was positively associated with later morning cortisol in females but not males.
Conclusion
Our results demonstrated sex differences in depressive mood among youth and the feasibility of psychobiological stress research in Morocco. More research is needed to identify sex-specific factors of depression and anxiety. Such effort would inform strategies to tailor treatment programs for females and males.
Glucocorticoids are believed to be crucial for understanding human aggression, psychopathologies, and crime because they can bridge adverse environmental events and the brain mechanisms of aggressive behavior, both acutely – i.e., while events unfold – and on the long run, by contributing to the epigenetic signature of toxic stressors over the lifetime. Yet, the role of glucocorticoids in human aggression is debated. There is one association that raises relatively little doubts; this is the one that links acute elevations in glucocorticoid secretion to aggressive responses, which indirectly supports the frustration–aggression hypothesis, one of the most popular psychological theories. Beyond its utility in psychology, this theory might also explain certain psychopathologies and emotional crime. The association of aggression with low glucocorticoid production by contrast is more disputed. Although demonstrated by many studies, the question remains open because the opposite association – high glucocorticoids–high aggression – is a similarly recurrent finding. It was suggested that contradictions may be solved by an approach sensitive to both the type of aggression and the psychopathology underlying aggression on one side and the glucocorticoid measures employed to study the phenomenon on the other. This chapter – already armed with the biological information presented in the previous one – aims at disentangling the intricate web of connections along this concept. The ultimate aim is to understand the acute and long-term alterations in glucocorticoid secretion in response to various types of stressors and the impact of the resulting glucocorticoid state on normal and abnormal human aggression. The neural consequences of altered glucocorticoid productions will also be addressed but briefly, because this will be dealt with in subsequent chapters.
Background
Allostatic load (AL) is a novel perspective for examining the damaging effects of stress on health and disease. Women veterans represent an understudied yet vulnerable subgroup of women with increased reports of traumatic stressors across their lifespan. AL has not been examined in this group. This study hypothesized that reports of sexual assault in childhood, civilian life, or in the military by women veterans was associated with AL and selected psychosocial measures. We also hypothesized that AL scores are positively associated with psychosocial characteristics.
Methods
Using a cross-sectional design, psychosocial and physiological data were obtained from women veterans (n = 81; 24–70 years old).
Findings
The AL score was 3.03 ± 2.36 and positively associated with age (p = .001). There was a trend for higher pain scores for women with an AL score of 2 or greater compared with those with an AL score of less than 2. There were significant differences in the Somatic Subscale of the Center for Epidemiological Depression Scale among the sexual assault categories with increasing scores among women reporting sexual assault in childhood, military, and civilian life (p = .049). The scores of the Profile of Mood States Depression/Dejection Subscale (p = .015), the Post-Traumatic Checklist- Military (p = .002), and the Pain Outcome Questionnaire (p = .001) were associated with sexual assault categories in a dose–response fashion.
Conclusions
AL was associated positively with age, and sexual assault categories were associated with increased somatization, depressed mood, posttraumatic symptoms and pain. Assessing both AL and sexual trauma are critical for preventing and managing the subsequent negative health consequences among women veterans.
Clinical theories posit interpersonal stress as an important factor in the emergence and exacerbation of depression and anxiety, while neuroendocrine research confirms the association of these syndromes with dysregulation in a major stress response system, the hypothalamic-pituitary-adrenal (HPA) axis. However, the proposal that depression and anxiety symptoms and diagnoses are associated with problematic HPA responses to close relationship stress has not been directly tested. We examined 196 heterosexual dating couples' depression and anxiety symptoms and diagnoses, assessed with questionnaires and diagnostic interviews, in relation to cortisol responses to discussion of an unresolved relationship conflict. Participants provided seven salivary samples in anticipation of and directly following the discussion, and throughout an hour-long recovery period, which were assayed for cortisol. Multilevel models of the HPA response predicted by symptoms or diagnoses showed that women's depressive symptoms predicted attenuated cortisol levels, with a flatter response curve. In contrast, men's depression symptoms and women's anxiety symptoms and diagnoses predicted higher cortisol levels. These findings highlight the importance of examining sex differences in responses to interpersonal stressors for understanding HPA dysregulation in internalizing psychopathology.
In all cultures in which they have been studied, exposure to and losses resulting from natural disasters are associated with increased prevalence of severe psychological distress, along with changes in activation of the limbic system (e.g., cortisol regulation) and changes in activation of the sympathetic nervous system. These patterns of psychological and physiological reactivity vary with the severity and duration of the attendant losses, biological sex, and psychosocial factors such as the reliability and attentiveness of available social partners. In this chapter, we review several biopsychosocial factors that have been found to covary with psychological distress and physiological stress reactivity in children and adolescents exposed to natural disasters. We then describe our own work examining psychosocial and biological correlates in children and adolescents who were displaced as a result of Hurricane Katrina (Vigil, Carle, Geary, Granger, Flinn, & Pendleton, 2009; Vigil & Geary, 2008; Vigil, Geary, Granger, & Flinn, 2010; Vigil & Brophy, in press). These studies show that exposure to natural disasters is associated with unique patterns of psychological functioning, social perceptions and behaviors, and physiological stress regulation, and that the patterns vary by social environment and biological sex. The studies also highlight the utility of assessing psychological and physiological stress responses outside of laboratory conditions and in individuals who have experienced chronic and pervasive stress.
Circadian rhythms maintain homeostasis of the body through hormonal, metabolic and cell cycle regulating cell proliferation. In turn, these are mediated by psychological conditions that may affect its operation and leave the body susceptible to diseases like cancer. The aim of this article is to review the relationship of circadian rhythms to cancer; with emphasis on those rhythms that are related to behaviors such as sleep-wake rhythm and the circadian rhythm of cortisol. This review will seek to identify, potential impact on the incidence and prognosis of cancer. Also psychobiological mechanisms that maintain the relationship between the circadian rhythms and cancer will be discussed.
The detection of stress at early stages is beneficial to both individuals and communities. However, traditional stress detection methods that use physiological signals are contact-based and require sensors to be in contact with test subjects for measurement. In this paper, we present a method to detect psychological stress in a non-contact manner using a human physiological response. In particular, we utilize a hyperspectral imaging (HSI) technique to extract the tissue oxygen saturation (StO2) value as a physiological feature for stress detection. Our experimental results indicate that this new feature may be independent from perspiration and ambient temperature. Trier Social Stress Tests (TSSTs) on 21 volunteers demonstrated a significant difference p\< 0.005 and a large practical discrimination (d 1/4 1.37) between normalized baseline and stress StO2 levels. The accuracy for stress recognition from baseline using a binary classifier was 76.19 and 88.1 percent for the automatic and manual selections of the classifier threshold, respectively. These results suggest that the StO2 level could serve as a new modality to recognize stress at standoff distances.
Evaluated the reliability and concurrent validity of the Center for Epidemiological Studies Depression Scale (CES-D). Two groups of Mexican students participated. The 1st group (
n = 66) was administered the Spanish version of the CES-D and 3 forms (E, F, & G) of the Spanish version of the Depression Adjective Check List (DACL). The 2nd group (
n = 82) was given the CES-D and the Spanish version of the Beck Depression Scale. The alpha coefficients were .86 and .80 for Groups 1 and 2 respectively. All Pearson correlations between the CES-D and the Beck and between the CES-D and the DACL were significant. It is concluded that the CES-D has adequate internal consistency reliability, test–retest reliability, and there are some data to demonstrate the concurrent validity. The CES-D appears useful for research in Mexico. (English abstract) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The measurement of cortisol in saliva provides the basic scientist as well as the clinician with a reliable tool for investigations of hypothalamus-pituitary-adrenal axis activity. Since saliva samples can be obtained stress-free and independent from medically trained personnel this method may be well suited for use in psychobiological studies. This overview intends to give a comprehensive introduction to the method of salivary cortisol assessment and to briefly discuss its application in different scientific disciplines.
The possibility that hypersecretion of corticotropin-releasing factor (CRF) contributes to the hyperactivity of the hypothalamo-pituitary-adrenal axis observed in patients with major depression was investigated by measuring the concentration of this peptide in cerebrospinal fluid of normal healthy volunteers and in drug-free patients with DSM-III diagnoses of major depression, schizophrenia, or dementia. When compared to the controls and the other diagnostic groups, the patients with major depression showed significantly increased cerebrospinal fluid concentrations of CRF-like immunoreactivity; in 11 of the 23 depressed patients this immunoreactivity was greater than the highest value in the normal controls. These findings are concordant with the hypothesis that CRF hypersecretion is, at least in part, responsible for the hyperactivity of the hypothalamo-pituitary-adrenal axis characteristic of major depression.
Four hundred thirty-eight subjects underwent an overnight dexamethasone suppression test (DST) to standardize the test for the diagnosis of melancholia (endogenous depression). Abnormal plasma cortisol concentrations within 24 hours after dexamethasone administration occurred almost exclusively in melancholic patients. The best plasma cortisol criterion concentration, above which a DST result may be considered abnormal, was 5 microgram/dL. The optimal dose of dexamethasone was 1 rather than 2 mg. Two blood samples obtained at 4 and 11 PM after dexamethasone administration detected 98% of the abnormal test results. This version of the DST identified melancholic patients with a sensitivity of 67% and a specificity of 96%. Baseline nocturnal plasma cortisol concentrations were not useful. Abnormal DST results were found with similar frequency among outpatients and inpatients with melancholia; but they were not related to age, sex, recent use of psychotropic drugs, or severity of depressive symptoms. Extensive evidence validates this practical test for the diagnosis of melancholia.
A Stress Inducing Speech Task was used to investigate the contribution of perceived stress, individual traits, and current mood states to individual differences in salivary cortisol responses. Additionally, we examined the correspondence between laboratory baseline cortisol levels and overall levels in daily life, and between cortisol responses to the speech task and a measure of stress reactivity to stressful events in daily life. Forty-two 'high stress' and forty-five 'low stress' white-collar males completed the speech task and an Experience Sampling study, in which stressful daily events and cortisol levels were monitored for five days. No association was found between perceived stress, trait anxiety, anger, depression, psychosomatic symptoms, coping style or personality and cortisol responses to the speech task. Negative mood state at baseline was associated with higher cortisol levels at baseline just before, and just after, the speech. Laboratory and field cortisol levels were moderately correlated, but no association was found between laboratory and field response measures. Laboratory baseline levels, but not responses to the speech task, were significant predictors of field cortisol levels.
This paper assesses the hypothesis that depressive syndrome is associated with socioeconomic status, using longitudinal data from the Baltimore Epidemiologic Catchment Area Followup. Socioeconomic measures include those used in most studies of status attainment, as well as measures of financial dependence, non-job income, and work environment. Analyses include inter- and intra-generational mobility, and replicate the basic aspects of the status attainment process, as well as psychiatric epidemiologic findings regarding gender, family history of depression, life events, and depressive syndrome. But the involvement of depressive syndrome in the process of status attainment, either as cause or consequence, is small and not statistically significant. There are strong effects of financial dependence and work environment on depressive syndrome. The findings shed doubt on the utility of the causation/selection/drift model for depression, to the extent it is based on linear relationships and socioeconomic rank at the macro level, while lending credibility to social-psychologically oriented theories of work environment, poverty, and depression.
Previous theories have emphasized the role of excessive glucocorticoid activity in the pathology of chronic stress. Nevertheless, insufficient glucocorticoid signaling (resulting from decreased hormone bioavailability or reduced hormone sensitivity) may have equally devastating effects on bodily function. Such effects may be related in part to the role of glucocorticoids in restraining activation of the immune system and other components of the stress response, including the sympathetic nervous system (SNS) and corticotropin-releasing hormone (CRH).
The literature on neuroendocrine function and glucocorticoid-relevant pathologies in stress-related neuropsychiatric disorders, including posttraumatic stress disorder and major depression, was reviewed.
Although not occurring together, both hypocortisolism and reduced responsiveness to glucocorticoids (as determined by dexamethasone challenge tests) were reliably found. Stress-related neuropsychiatric disorders were also associated with immune system activation/inflammation, high SNS tone, and CRH hypersecretion, which are all consistent with insufficient glucocorticoid-mediated regulation of stress hyperresponsiveness. Finally, antidepressants, a mainstay in the treatment of stress-related disorders, were regularly associated with evidence of enhanced glucocorticoid signaling.
Neuroendocrine data provide evidence of insufficient glucocorticoid signaling in stress-related neuropsychiatric disorders. Impaired feedback regulation of relevant stress responses, especially immune activation/inflammation, may, in turn, contribute to stress-related pathology, including alterations in behavior, insulin sensitivity, bone metabolism, and acquired immune responses. From an evolutionary perspective, reduced glucocorticoid signaling, whether achieved at the level of the hormone or its receptor, may foster immune readiness and increase arousal. Emphasis on insufficient glucocorticoid signaling in stress-related pathology encourages development of therapeutic strategies to enhance glucocorticoid signaling pathways.
Abnormal responses of the hypothalamic-pituitary-adrenal (HPA) axis to stress are thought to be involved in the pathophysiology of major depressive disorder (MDD). The aim of the present study was to determine whether cortisol responses to negative and positive daily events in depressed participants (N= 47) differed from such responses in healthy participants (N= 39). We also examined the influence of clinical characteristics and possible gender differences in cortisol responses to events. Finally, the role of mood changes in mediating cortisol responses was assessed.
Experience sampling methodology (self-reports of mood and events, with simultaneous saliva samples, 10 times each day for 6 consecutive days) and multilevel regression analysis were used to examine the relationship between events in daily life and salivary cortisol levels.
In contrast to healthy participants, depressed participants showed no increase in cortisol following negative events. Responses were even more blunted in depressed participants with a family history of mood disorders. Although the effects of negative events on cortisol responses appeared to be mediated by changes in mood, negative affect tended to be less closely associated with cortisol levels in depressed participants. Depressed women showed larger cortisol responses to negative events than depressed men. Positive events had no effect on cortisol levels in either group.
These results suggest that responses of the HPA axis to negative daily events and mood changes are blunted in MDD. Future studies will need to address whether these abnormalities disappear after clinical recovery.
This meta-analysis reviews 208 laboratory studies of acute psychological stressors and tests a theoretical model delineating conditions capable of eliciting cortisol responses. Psychological stressors increased cortisol levels; however, effects varied widely across tasks. Consistent with the theoretical model, motivated performance tasks elicited cortisol responses if they were uncontrollable or characterized by social-evaluative threat (task performance could be negatively judged by others), when methodological factors and other stressor characteristics were controlled for. Tasks containing both uncontrollable and social-evaluative elements were associated with the largest cortisol and adrenocorticotropin hormone changes and the longest times to recovery. These findings are consistent with the animal literature on the physiological effects of uncontrollable social threat and contradict the belief that cortisol is responsive to all types of stressors.
SAS PROC MIXED is a flexible program suitable for fitting multilevel models, hierarchical linear models, and individual growth models. Its position as an integrated program within the SAS statistical package makes it an ideal choice for empirical researchers and applied statisticians seeking to do data reduction, management, and analysis within a single statistical package. Because the program was developed from the perspective of a "mixed" statistical model with both random and fixed effects, its syntax and programming logic may appear unfamiliar to users in education and the social and behavioral sciences who tend to express these models as multilevel or hierarchical models. The purpose of this paper is to help users familiar with fitting multilevel models using other statistical packages (e.g., HLM, MLwiN, MIXREG) add SAS PROC MIXED to their array of analytic options. The paper is written as a step-by-step tutorial that shows how to fit the two most common multilevel models: (a) school effects models, designed for data on individuals nested within naturally occurring hierarchies (e.g., students within classes); and (b) individual growth models, designed for exploring longitudinal data (on individuals) over time. The conclusion discusses how these ideas can be extended straighforwardly to the case of three level models. An appendix presents general strategies for working with multilevel data in SAS and for creating data sets at several levels.
• We studied disturbances in the circadian pattern of plasma corticotropin and cortisol concentrations in 25 depressed patients (eight dexamethasone suppression test [DST] nonsuppressors and 17 suppressors) and 21 normal control subjects. Blood samples were drawn every 20 minutes for 24 hours before the administration of dexamethasone, and for a second 24 hours after the administration of 1 mg of dexamethasone. The corticotropin and cortisol level rhythms were examined using three different statistical methods. Nonsuppressors averaged greater elevations in plasma cortisol and corticotropin levels than did subjects in the other two groups, both before and after administration of the dexamethasone. The cortisol levels of the suppressors were virtually identical to those of the control subjects. However, the suppressors had significant elevations of corticotropin levels compared with normal control subjects, especially on the day before taking dexamethasone. Before taking dexamethasone, the depressed patients reached a daily nadir of cortisol concentration approximately two hours earlier than did the normal control subjects. The DST nonsuppressors also exhibited a blunting in the expected circadian rhythm of the corticotropin level.
SAS PROC MIXED is a flexible program suitable for fitting multilevel models, hierarchical linear models, and individual growth models. Its position as an integrated program within the SAS statistical package makes it an ideal choice for empirical researchers and applied statisticians seeking to do data reduction, management, and analysis within a single statistical package. Because the program was developed from the perspective of a "mixed" statistical model with both random and fixed effects, its syntax and programming logic may appear unfamiliar to users in education and the social and behavioral sciences who tend to express these models as multilevel or hierarchical models. The purpose of this paper is to help users familiar with fitting multilevel models using other statistical packages (e.g., HLM, MLwiN, MIXREG) add SAS PROC MIXED to their array of analytic options. The paper is written as a step-by-step tutorial that shows how to fit the two most common multilevel models: (a) school effects models, designed for data on individuals nested within naturally occurring hierarchies (e.g., students within classes); and (b) individual growth models, designed for exploring longitudinal data (on individuals) over time. The conclusion discusses how these ideas can be extended straighforwardly to the case of three level models. An appendix presents general strategies for working with multilevel data in SAS and for creating data sets at several levels.
This study investigated the relations among depression, acculturation, and socioeconomic status (SES) in a young-adult Latino sample. Data were obtained from 1,271 Latino first-year college students; 89% self-labeled as either Mexican American or Hispanic, and 11% as Mexican National. Symptoms of depression were compared for various acculturation levels, and bicultural groups with controls for SES and gender. The Acculturation Rating Scale for Mexican Americans-II (ARSMA-II) was used to assess acculturation characteristics. Clinical depression and symptoms of depression were measured using the DSD26 Symptom Scale for assessment of depressive symptoms and major depression. Variance in depression scores was found to be influenced more by gender and SES than by acculturation or ethnic identity status. Assimilated Mexican Americans reported significantly fewer symptoms of depression than their more traditional counterparts. Ethnicity and acculturation per se were not found to lessen or increase riskfordepression, but SES associated with ethnicity wasfound to directly affect depression scores.
The CES-D scale is a short self-report scale designed to measure depressive symptomatology in the general population. The items of the scale are symptoms associated with depression which have been used in previously validated longer scales. The new scale was tested in household interview surveys and in psychiatric settings. It was found to have very high internal consistency and adequate test- retest repeatability. Validity was established by pat terns of correlations with other self-report measures, by correlations with clinical ratings of depression, and by relationships with other variables which support its construct validity. Reliability, validity, and factor structure were similar across a wide variety of demographic characteristics in the general population samples tested. The scale should be a useful tool for epidemiologic studies of de pression.
This article examines low socioeconomic staus (SES) as both a cause and a consequence of mental illnesses by investigating the mutual influence of mental disorders and educational attainment, a core element of SES. The analyses are based on a longitudinal panel design and focus on four disorders: anxiety, depression, antisocial disorder, and attention deficit disorder. The article shows that each disorder has a unique relationship with SES, highlighting the need for greater consideration of antisocial disorders in the status attainment process and for further theoretical development in the sociology of mental disorders to account for disorder-specific relations with SES.
Critiques T. Pincus and L. Callahan's (see PA, Vol 82: 29254) hypothesis that low SES is not just a surrogate marker; it is itself a contributor to and determinant of the development of psychosocial characteristics that lead to ill health via biobehavioral processes. Various psychosocial risk factors like depression, hostile personality, social isolation, and jobs that impose high demands with low decisions, lead to low serotonin functioning in the central nervous system, making both animals and humans prone to various health problems. Psychosocial, behavioral and pharmacological points for interventions are suggested. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The construct validity of a Chinese-language version of the Center for Epidemiological Studies Depression Scale (CES-D; Radloff, 1977) was tested on a sample of 138 Hong Kong Chinese married couples. Confirmatory factor analysis identified 2 factors: (a) depressive symptom factors and (b) interpersonal problem factors. Those factors attained convergent, discriminant, and structural validity when evaluated against social desirability. The CES-D also manifested nomological validity in terms of its significant relationships with measures of life satisfaction and stressful life events.
This article reviews the evidence for differing rates of depression between the sexes in the United States and elsewhere during the last 40 years, and then critically analyzes the various explanations offered. These explanations include the possibility that the trends are spurious because of artifacts produced by methods of reporting symptoms, or that they are real because of biological susceptibility (possibly genetic or female endocrine), psychosocial factors such as social discrimination, or female-learned helplessness.
Patients with severe depressive illnesses of the endogenomorphic type frequently manifest several hormonal abnormalities. The best documented are the hypersecretion of cortisol, particularly in the late evening and early morning, associated with relative resistance to dexamethasone suppression; diminished or absent HGH responses to insulin-induced hypoglycemia; and diminished TSH responses to TRH. There are also reports from one laboratory of relatively diminished plasma LH concentration in postmenopausal women with primary unipolar depressive illness, a finding that awaits replication by other centers. Most of these hormonal abnormalities provide further support to the concept of hypothalamic dysfunction in certain forms of depressive illness, and are consistent with current hypotheses of abnormal brain monoamine activity in these conditions. These studies suggest that analysis of neuroendocrine responses in patients with mental illnesses may be a valuable tool for the study of possible alterations in brain function. Further advances may be expected when radioimmunoassay techniques become available for the hypothalamic releasing and inhibiting factors themselves.
Severity of depression, as reflected by total scores on depression rating scales, has been established as one of several major sources of variance associated with hypothalamic-pituitary-adrenal axis dysregulation in patients with major depressive disorder. To determine which of the symptoms comprising clinically defined severity of illness contribute most to this relationship, we studied the associations between postdexamethasone plasma cortisol levels and components of the Hamilton Rating Scale for Depression (HRSD) in 114 patients with major depressive disorder. At pretreatment baseline, severity of depression was modestly but significantly correlated with postdexamethasone plasma cortisol; a large part of this relationship was associated with the anxiety components of the HRSD. When relationships between postdexamethasone plasma cortisol and severity measures were studied longitudinally during treatment, this contribution of the anxiety items persisted. The anxiety associated with depression appears to be a major clinical factor associated with the hypothalamic-pituitary-adrenal axis dysregulation in major depressive disorder.
We studied disturbances in the circadian pattern of plasma corticotropin and cortisol concentrations in 25 depressed patients (eight dexamethasone suppression test [DST] nonsuppressors and 17 suppressors) and 21 normal control subjects. Blood samples were drawn every 20 minutes for 24 hours before the administration of dexamethasone, and for a second 24 hours after the administration of 1 mg of dexamethasone. The corticotropin and cortisol level rhythms were examined using three different statistical methods. Nonsuppressors averaged greater elevations in plasma cortisol and corticotropin levels than did subjects in the other two groups, both before and after administration of the dexamethasone. The cortisol levels of the suppressors were virtually identical to those of the control subjects. However, the suppressors had significant elevations of corticotropin levels compared with normal control subjects, especially on the day before taking dexamethasone. Before taking dexamethasone, the depressed patients reached a daily nadir of cortisol concentration approximately two hours earlier than did the normal control subjects. The DST nonsuppressors also exhibited a blunting in the expected circadian rhythm of the corticotropin level.
Primary depression can be associated with substantial hypercortisolism, thus prompting some researchers to suggest that depression shares pathophysiologic features with Cushing's disease. Clinically, depression can be difficult or impossible to distinguish from mild or early Cushing's disease that is associated with depressive features. The purpose of this study was to evaluate whether the pituitary-adrenal responses to ovine corticotropin-releasing hormone could help to clarify the mechanism of hypercortisolism in depression and in Cushing's disease and to assist in the differential diagnosis of these disorders. As compared with controls (n = 34), depressed patients (n = 30) had basal hypercortisolism (P less than 0.001) that was associated with attenuated plasma ACTH responses to ovine corticotropin-releasing hormone (P less than 0.001). This indicates that in patients with depression, the corticotroph cell in the pituitary responds appropriately to the negative feedback of high cortisol levels. In contrast, patients with Cushing's disease (n = 29) had plasma ACTH hyperresponsiveness to ovine corticotropin-releasing hormone (P less than 0.001), despite basal hypercortisolism (P less than 0.001), which indicates a gross impairment of the mechanism by which cortisol exerts negative feedback on the pituitary. Less than 25 percent of the patients with depression or Cushing's disease had peak ACTH responses that overlapped. We conclude that the pathophysiologic features of hypercortisolism in depression and Cushing's disease are distinct in each of the disorders and that the ovine corticotropin-releasing hormone stimulation test can be helpful in their differential diagnosis.
Thousands of studies have been conducted of the functioning of the many neurotransmitter systems in order to explore the biologic basis of major depressive disorder. Instead of reviewing this literature exhaustively, we have attempted to propose a model that accommodates the clinical observation that chronic stress early in life in vulnerable persons predisposes them to major depression with contemporary observations of the potential consequences of repeated central nervous system exposure to effectors of the stress response. This model accords with current clinical judgment that major depression is best treated with a combination of psychopharmacologic agents and psychotherapy. Accordingly, whereas psychopharmacologic intervention may be required to resolve an active episode of major depression and to prevent recurrences, psychotherapy may be equally important to lessen the burden of stress imposed by intense inner conflict and counterproductive defenses.
The 1 mg and 2 mg dexamethasone suppression tests (DST) were evaluated in two groups of endogenously depressed patients (n = 39 and n = 30, respectively) who also had a 1300-1600 hr basal cortisol assessment. Non-suppressors (on both DSTs) had significantly higher basal plasma cortisol levels and thus were significantly associated with relative cortisol hypersecretion. However, there was only a partial overlap between DST response and basal plasma cortisol, with a large variation of cortisol levels among non-suppressors. The 2 mg DST appears to be more specific for cortisol hypersecretion than the 1 mg DST. If cortisol hypersecretion is to be identified, neither the 1 mg or 2 mg DST is an adequate assessment nor a substitute for a basal cortisol assessment.
Plasma levels of cortisol were sampled for 24 hours in 32 endogenously depressed (ED) patients and 72 normal controls who also underwent the dexamethasone suppression test. The ED patients had significantly higher mean 24-hour plasma levels of cortisol (means 24h PC). However, means 24h PC values of subjects in both groups were normally distributed, with a marked overlap between the two. Only seven ED patients had means 24h PC values higher than 2 SDs from the normal mean (greater than 10 micrograms/dL). An abnormal dexamethasone suppression test result was only partially related to basal cortisol levels. The mean plasma level of cortisol between 1 and 4 PM was found to be highly correlated with the means 24h PC value in ED patients, as has been previously reported in normal subjects and patients with various other diseases (in which it also powerfully discriminated between hypersecretors and normosecretors). This finding supports the use of mean cortisol levels between 1 and 4 PM as a reliable and convenient indication of cortisol secretion.
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To the Editor: The recent availability of the newly sequenced human corticotropin-releasing factor holds promise in furthering the understanding of the pathophysiology underlying hypercortisolism linked to depression.¹ Current research suggests that corticotropin-releasing factor is not only a key hormone in the regulation of corticotropin but may also act in the brain to initiate a variety of physiologic responses characteristic for stress.² We have compared the secretory patterns of cortisol with the corticotropin and Cortisol responses to human corticotropin-releasing factor in 12 unmedicated patients (aged 36 to 69) with a major depressive disorder (primary and endogenous) and 9 healthy controls (aged . . .
This paper presents evidence from three samples, two of college students and one of participants in a community smoking-cessation program, for the reliability and validity of a 14-item instrument, the Perceived Stress Scale (PSS), designed to measure the degree to which situations in one's life are appraised as stressful. The PSS showed adequate reliability and, as predicted, was correlated with life-event scores, depressive and physical symptomatology, utilization of health services, social anxiety, and smoking-reduction maintenance. In all comparisons, the PSS was a better predictor of the outcome in question than were life-event scores. When compared to a depressive symptomatology scale, the PSS was found to measure a different and independently predictive construct. Additional data indicate adequate reliability and validity of a four-item version of the PSS for telephone interviews. The PSS is suggested for examining the role of nonspecific appraised stress in the etiology of disease and behavioral disorders and as an outcome measure of experienced levels of stress.
