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

Abstract

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...

Biological Basis of Depression in Adults with Diabetes

“…Interestingly, this association was not noted in patients without coronary heart disease [16]. Contrary to this, Conrad et al [17] did not note any significant differences in salivary cortisol diurnal variation among 46 depressed subjects at risk for cardiovascular disease compared to 19 subjects without depression.…”

“…Cortisol awakening response Huber et al [12] ↓ Awakening cortisol rise in depressed compared with nondepressed Kuehner et al [11] ↓ CAR in those with increased vulnerability to depression Diurnal cortisol profile Van den Bergh et al [14,15] Flatter diurnal cortisol profile with depressive symptoms and increased emotional distress Bhattacharyya et al [16] Flatter diurnal cortisol profile in more depressed Conrad et al [17] No association between depression and diurnal cortisol profile…”

Depression, heart rate related variables and cardiovascular disease

“…When depressive participants were alone they evidenced lower HRV and higher negative affect, but not when they were engaged in social interactions with a partner, family members, or friends. Conrad et al (2008) found no differences in HRV (measured as RSA adjusted for respiration, LF, VLF during the day between depressed and non-depressed older individuals at risk for CVD (social context was not examined.) An individual's fitness is an important possible mediator of the relationship between depression and HRV.…”

Emotional reactivity to daily events in major and minor depression.

“…Horan, Green, Kring, and Nuechterlein (2006) found that schizophrenics who reported trait anhedonia on questionnaires did not differ from controls on in vivo hedonic responses to film clips and pleasurable food items. Likewise, Conrad, Wilhelm, Roth, Spiegel, and Taylor (2008) found that although depressed and nondepressed at risk for heart disease have been shown to differ on a laboratory Stressor task (Taylor et al, 2006), these findings were not replicated in daily life, even after controlling for respiration and physical activity. To better isolate both the nature and the source of the divergence, as well as its meaning, clearly it will be useful for studies to acquire laboratory and real-life data from the same individuals and/or to embed controlled stimuli into ESM designs to "calibrate" emotion reactivity (for a longer discussion, see Bylsma & Rottenberg, 2011).…”