Cortisol Circadian Rhythm Alterations in Psychotic Major Depression

Keller, Jennifer; Flores, Benjamin; Gomez, Rowena; Solvason, H. Brent; Kenna, Heather A.; Williams, Gordon H.; Schatzberg, Alan F.

doi:10.1016/j.biopsych.2005.10.014

Cited by 186 publications

(102 citation statements)

References 44 publications

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“…This finding is in line with findings of elevated evening salivary cortisol in depression in 8-to 16-year olds (Goodyer et al, 1996), in 13-to 17-year olds (Goodyer et al, 2001), in adolescents having reached Tanner stage III (Dahl et al, 1991;Rao et al, 1996;Forbes et al, 2006) and in patients with severe depression or psychotic depression (Keller et al, 2006). However, these results do not corroborate the findings of Vedhara and colleagues (2003), who did not find associations between indices of emotional distress and absolute levels of cortisol on any time of the day, and the findings of Adam (2006) who, in a study of normal adolescents, did not found associations between trait anxiety and any of the diurnal cortisol parameters.…”

Section: Discussionsupporting

confidence: 91%

Self-reported symptoms of depressed mood, trait anxiety and aggressive behavior in post-pubertal adolescents: Associations with diurnal cortisol profiles

Bergh

Calster

Puissant

et al. 2008

Hormones and Behavior

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Self-reported symptoms of depressed mood, trait anxiety and aggressive behavior in post-pubertal adolescents Van Den Bergh, Bea; van Calster, B.; Lagae, L.; Van Huffel, S. Published in: Hormones and Behavior Publication date: 2008 Link to publication Citation for published version (APA):Van den Bergh, B. R. H., van Calster, B., Lagae, L., & Van Huffel, S. (2008). Self-reported symptoms of depressed mood, trait anxiety and aggressive behavior in post-pubertal adolescents: associations with diurnal cortisol profiles. Hormones and Behavior, 54(2), 253-257. General rightsCopyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.-Users may download and print one copy of any publication from the public portal for the purpose of private study or research -You may not further distribute the material or use it for any profit-making activity or commercial gain -You may freely distribute the URL identifying the publication in the public portal Take down policyIf you believe that this document breaches copyright, please contact us providing details, and we will remove access to the work immediately and investigate your claim. The association between self-reported symptoms and diurnal cortisol profiles was studied in post-puberty adolescents (29 boys and 29 girls, M age = 15.06 years). The adolescents completed the Children's Depression Inventory, State Trait Anxiety Inventory, and an Aggressive behavior scale. The diurnal cortisol profile was derived from three saliva samples, collected at awakening, noon and evening on a week-end day. Univariate repeated measurement regressions revealed that depressed mood and trait anxiety were strongly and aggressive behavior was weakly related to the diurnal cortisol profile: greater emotional distress was associated with flatter diurnal cortisol profiles. Multivariate analysis, however, revealed that only trait anxiety made an independent contribution. Further analyses suggested that trait anxiety was related to elevated evening cortisol rather than to decreased awakening cortisol and that from a trait anxiety score of 38 onwards, high anxious adolescents show clearly higher evening cortisol than low anxious adolescents. These data suggest that anxiety disorder comorbidity might explain some of the differences in HPA-axis function among depressed patients. A B S T R A C T A R T I C L E I N F O

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Section: Discussionsupporting

confidence: 91%

Self-reported symptoms of depressed mood, trait anxiety and aggressive behavior in post-pubertal adolescents: Associations with diurnal cortisol profiles

Bergh

Calster

Puissant

et al. 2008

Hormones and Behavior

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“…Maes and colleagues (1994) suggested that increased activation of the HPA-axis is more prominent in severe than moderate depression. Further, hypercortisolism in depression has been most consistently found in subjects with "severe forms of depression", for instance those with psychotic features (Keller et al, 2006), which none of our subjects had, or with melancholia (Gold & Chrousos, 2002;Stewart, Quitkin, McGrath, & Klein, 2005). Nonpsychotic subjects with more moderate levels of depression may not show hypercortisolemia (Keller et al, 2006).…”

Section: Discussionmentioning

confidence: 53%

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

Conrad

Wilhelm

Roth

et al. 2008

Journal of Psychiatric Research

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

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“…Whatever the eventual explanation, the findings in this paper may have clinical significance. A substantial proportion (c. 50%) of patients with major depression also show attenuated or flattened diurnal rhythms in cortisol (Bridges and Jones, 1966;Keller et al, 2006;von Zerssen et al, 1987). Increased neurogenesis in the dentate has been related to the therapeutic response to anti-depressants (Malberg et al, 2000;Santarelli et al, 2003;Sapolsky, 2004), although a recent paper reports no association between Ki-67 labelling and depression in the human dentate gyrus (Reif et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Interactions between Nitric Oxide and Corticosterone in the Regulation of Progenitor Cell Proliferation in the Dentate Gyrus of the Adult Rat

Pinnock

Balendra

Chan

et al. 2006

Neuropsychopharmacol

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It is well established that L-NAME, a generic NOS inhibitor, stimulates neurogenesis in the dentate gyrus of the adult rat and corticosterone reduces it. These experiments explore the interaction between L-NAME and corticosterone. L-NAME (50 mg/kg), as expected, increased proliferation, but also lowered plasma corticosterone levels. However, the stimulating action of L-NAME depends on the presence of rhythmic changes in plasma corticosterone, as it is abolished in rats treated with a subcutaneous implant of corticosterone, which flattens the diurnal rhythm. Adrenalectomized rats implanted with corticosterone also failed to respond to L-NAME. Giving them a single daily injection of corticosterone (2 mg/kg) in an attempt to replicate the diurnal rhythm restored the sensitivity of the progenitor cells to L-NAME. The mechanism for this result remains to be investigated. Excess corticosterone given by daily injection (40/mg/kg) reduced proliferation but did not alter the response to L-NAME, even though this occurred from a lower baseline. nNOS was demonstrable only in the inner (proliferative) layer of the dentate gyrus in control rats, and did not alter following excess corticosterone treatment. iNOS was detectable at low levels in control rats, but was increased markedly following corticosterone. eNOS was evident throughout the dentate gyrus, and also increased after corticosterone (particularly in the hilus). Aminoguanidine (100 mg/kg/day; an iNOS antagonist) significantly increased proliferation in corticosterone-treated rats (40 mg/kg/day) but not in controls without additional corticosterone, confirming that iNOS plays a role in corticosterone-regulated neurogenesis. Corticosterone may thus act on progenitor cells in part at least through increased nitric oxide (NO) formation. The effects of reduced NO on neurogenesis may rely on a dual mechanism: corresponding reductions in plasma corticosterone and increased induction of iNOS (and/or eNOS) within the dentate gyrus. The possibility that NO acts downstream of glucocorticoids in the dentate gyrus is suggested.

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Cortisol Circadian Rhythm Alterations in Psychotic Major Depression

Cited by 186 publications

References 44 publications

Self-reported symptoms of depressed mood, trait anxiety and aggressive behavior in post-pubertal adolescents: Associations with diurnal cortisol profiles

Self-reported symptoms of depressed mood, trait anxiety and aggressive behavior in post-pubertal adolescents: Associations with diurnal cortisol profiles

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

Interactions between Nitric Oxide and Corticosterone in the Regulation of Progenitor Cell Proliferation in the Dentate Gyrus of the Adult Rat

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