Adrenomedullary function in depressed patients

doi:10.1016/0022-3956(94)90018-3

Journal of Psychiatric Research

Volume 28, Issue 4, July–August 1994, Pages 357-367

https://doi.org/10.1016/0022-3956(94)90018-3 Get rights and content

Abstract

In this paper from the Collaborative Depression Study (CDS)—Biological, a set of data analyses are presented which indicate that depressed states and perhaps depressed mood are associated with a greater activation of the adrenomedullary system than the sympathetic nervous system [as measured by norepinephrine (NE) and normetanephrine excretion]. For the most part this finding of predominant activation of the adrenomedullary system is seen in unipolar and not bipolar patients.

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Depression is linked to increased platelet activation and hypercoagulability (Kop et al 2002; Kuijpers et al 2002; Laghrissi-Thode et al 1997; Lederbogen et al 2001; Musselman et al 1996, 2002; von Känel et al 2001). Evidence suggests depression-related alterations in neurohormonal mechanisms, such as hypothalamic-pituitary-adrenal (HPA) axis hyperactivity and increases in plasma cortisol (Ehlert et al 2001; Maas et al 1994; Plotsky et al 1998), might correlate with increased CHF risk (Francis et al 1993; Pepper and Lee 1999). Behavioral factors also increase risk for cardiac disease for patients with depression who might not adhere to smoking cessation goals, dietary changes, daily aspirin therapy, antihypertensive regimens, or cardiac rehabilitation (Anda et al 1990; Blumenthal et al 1982; Carney et al 1995; Glazer et al 2002; Wang et al 2002).
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Studies have consistently documented hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis in depressed patients, as reflected by hypercortisolemia, elevated corticotropin-releasing factor in cerebrospinal fluid, decreased adrenocorticotropic hormone response to corticotropin-releasing factor challenge, nonsuppression of cortisol secretion in response to dexamethasone, and pituitary and adrenal gland enlargement (see review36–39). HPA hyperactivity in turn augments sympathetic hyperactivity via central regulatory pathways; this phenomenon has been demonstrated in depressed patients, manifest by elevated plasma norepinephrine as well as a hypersecretory catecholamine response to orthostatic challenge.40,41 However, not all studies have found this association; a report by Carney et al suggested no relationship between norepinephrine levels and depression in a study of 89 patients with CAD (norepinephrine levels for depressed versus nondepressed patients: 280 pg/mL versus 323 pg/mL, values log10 transformed, P = .36).42
Depression is 4 to 5 times as common in heart failure (HF) patients as in the general population, might confer a higher risk of developing HF, and negatively affects prognosis in established HF.
A review was undertaken via Medline (1966–2003) and PsycINFO (1872–2003) searches using the subject headings “depressive disorder” and “heart failure, congestive.” Our findings suggest that the link between depression and HF may be due to shared pathophysiology. Depression may augment catecholamine release, arrhythmias, elaboration of proinflammatory cytokines, and platelet activation—processes that may influence prognosis in HF. Depression is also associated with a higher risk of noncompliance and lower levels of social support, which have been shown to worsen prognosis in HF. The impact of pharmacologic or behavioral treatment for depression on physiologic parameters or clinical outcomes in HF remains unclear. Inherent difficulties in recognition of depression in the setting of HF may decrease the likelihood that depressed patients receive the treatment they need.
Depression is common in HF, may contribute to the development of HF in susceptible populations, and is independently predictive of poor clinical outcomes. Pathophysiologic pathways and psychosocial issues that are shared between the 2 conditions might explain these observations and represent potential therapeutic targets. Vigilant attention to the recognition and treatment of depression in HF patients is warranted.
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Citation Excerpt :
Studies have consistently documented HPA hyperactivity in depressed patients, as reflected by elevated corticotropin-releasing factor (CRF) in cerebrospinal fluid, decreased adrenocorticotropic hormone (ACTH) response to CRF challenge, nonsuppression of cortisol secretion in response to dexamethasone, hypercortisolemia, and pituitary and adrenal gland enlargement (for review, see Plotsky et al 1998; Arborelius et al 1999; Ehlert et al 2001). Sympathoadrenal hyperactivity has also been demonstrated in depressed patients, manifest by elevated plasma norepinephrine as well as a hypersecretory catecholamine response to orthostatic challenge (Gold et al 2000; Maas et al 1994), although not all studies have found this association (Carney et al 1999). Therefore, HPA and SA hyperactivity may speed the development of CVD and worsen prognosis for patients with underlying CVD.
This article explores the relationship between depression and cardiovascular disease from a mechanistic standpoint. Depression and cardiovascular disease are two of the most prevalent health problems in the United States and are the two leading causes of disability both in the United States and worldwide. Although depression is a known risk factor for the development of cardiovascular disease, as well as an independent predictor of poor prognosis following a cardiac event, the mechanistic relationship between the two remains unclear. Depression is associated with changes in an individual's health status that may influence the development and course of cardiovascular disease, including noncompliance with medical recommendations, as well as the presence of cardiovascular risk factors such as smoking and hypertension. In addition, depression is associated with physiologic changes, including nervous system activation, cardiac rhythm disturbances, systemic and localized inflammation, and hypercoagulability, that negatively influence the cardiovascular system. Further, stress may be an underlying trigger that leads to the development of both depression and cardiovascular disease. This article reviews seven potential mechanisms for the relationship between depression and cardiovascular disease and presents the available evidence surrounding each mechanism. Finally, future directions for research are discussed.

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^☆: This program was carried out with the cooperation and participation of the Collaborative Program Investigators and Institutions: S.H. Koslow (Project Director), S. Secunda (Deputy Project Director), I. Hanin (Consultant), B. Harris (Protocol Monitor), National Institute of Mental Health; M.M. Katz (Co-Chairman) Albert Einstein College of Medicine; J.W. Maas (Co-Chairman), C. Bowden, R. Schulman, The University of Texas Health Science Center at San Antonio; D.E. Redmond, Jr, Yale University School of Medicine; A. Swann, The University of Texas Health Science Center at Houston; J.M. Davis, S. Chang, D. Garver, J. Javaid, Illinois State Psychiatric Institute; R. Casper, Michael Reese Hospital and Medical Center; J. Mendels, D. Brunswick, A. Frazer, A. Ramsey, S. Stern, Philadelphia VA Medical Center; P.E. Stokes, J. Kocsis, Cornell University Medical College; E. Robins, J. Croughan, Washington University School of Medicine; Nancy Berman, Harbor-UCLA Medical Center. The research was supported by grants UO1 MH38084, UO1 MH26977, UO1 MH26979, UO1 MH26978, UO1 MH31921, and UO1 MH36232.

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Adrenomedullary function in depressed patients☆

Abstract

Analytical Chemistry

Analytical Biochemistry

Psychiatry Research

Brain peptide regulation of adrenal epinephrine secretion

American Journal of Psysiology

Corticotropin-releasing factor: effects on the automatic nervous system and visceral systems

Federation Proceedings

Cerebrospinal fluid and urinary biogenic amines in depressed patients and healthy controls

Archives of General Psychiatry

Physostigmine-induced epinephrine release in patients with affective disorder

American Journal of Psychiatry

Video methodology for research in psychopathology and psychopharmacology

Archives of General Psychiatry

A multivantage approach to measurement of behavioral and affect states for clinical and psychobiological research

Psychological Reports

Behavioral measurement and drug response characteristics of unipolar and bipolar depression

Psychological Medicine

Video methodologies in study of the patient and treatment of depression

Psych Annals

Depressive behavior and hyperactive adrenocortical function

American Journal of Psychiatry

CSF and urinary biogenic amines and metabolites in depression and mania

Archives of General Psychiatry

Plasma noradrenaline concentrations in blood pressure in essential hypertension, pheochromocytoma, and depression

Clinical Science and Molecular Medicine

Biological component of the NIMH clinical research branch collaborative program on the psychobiology of depression; I. Background and theoretical cons iderations

Psychological Medicine