Salivary cortisol and α-amylase: subclinical indicators of stress as
cardiometabolic risk

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Abstract

Currently, the potential for cardiovascular (CV) stress-induced risk is primarily based on the theoretical (obvious) side effects of stress on the CV system. Salivary cortisol and α-amylase, produced respectively by the hypothalamus-pituitary-adrenal (HPA) axis and the sympathetic-adrenomedullary (SAM) system during stress response, are still not included in the routine evaluation of CV risk and require additional and definitive validation. Therefore, this article overviews studies published between 2010 and 2015, in which salivary cortisol and α-amylase were measured as stress biomarkers to examine their associations with CV/CMR (cardiometabolic risk) clinical and subclinical indicators. A comprehensive search of PubMed, Web of Science and Scopus electronic databases was performed, and 54 key articles related to the use of salivary cortisol and α-amylase as subclinical indicators of stress and CV/CMR factors, including studies that emphasized methodological biases that could influence the accuracy of study outcomes, were ultimately identified. Overall, the biological impact of stress measured by salivary cortisol and α-amylase was associated with CV/CMR factors. Results supported the use of salivary cortisol and α-amylase as potential diagnostic tools for detecting stress-induced cardiac diseases and especially to describe the mechanisms by which stress potentially contributes to the pathogenesis and outcomes of CV diseases.

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Most cited references 84

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Salivary cortisol as a biomarker in stress research.

Dirk Hellhammer, Stefan Wüst, Brigitte Kudielka (2009)

Salivary cortisol is frequently used as a biomarker of psychological stress. However, psychobiological mechanisms, which trigger the hypothalamus-pituitary-adrenal axis (HPAA) can only indirectly be assessed by salivary cortisol measures. The different instances that control HPAA reactivity (hippocampus, hypothalamus, pituitary, adrenals) and their respective modulators, receptors, or binding proteins, may all affect salivary cortisol measures. Thus, a linear relationship with measures of plasma ACTH and cortisol in blood or urine does not necessarily exist. This is particularly true under response conditions. The present paper addresses several psychological and biological variables, which may account for such dissociations, and aims to help researchers to rate the validity and psychobiological significance of salivary cortisol as an HPAA biomarker of stress in their experiments.

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Heather M Burke, Mary C Davis, Christian Otte … (2005)

The purpose of this meta-analysis is to examine the association between depression and cortisol responses to psychological stressors. A total of seven studies comparing plasma or cortisol responses to psychological stressors in clinically depressed (MDD) and non-depressed (ND) individuals (N = 196: 98 MDD, 98 ND; 83 men, 113 women; mean age = 40 years) were included. Sample size-adjusted effect sizes (Cohen's d statistic) were calculated and averaged across baseline (before stressor onset), stress (stressor onset up to 25 min after stressor offset), and recovery (more than 25 min after stressor offset) periods. Overall, MDD and ND individuals exhibited similar baseline and stress cortisol levels, but MDD patients had much higher cortisol levels during the recovery period than their ND counterparts. There was also a significant time of day effect in which afternoon studies were more likely to reveal higher baseline cortisol levels, blunted stress reactivity, and impaired recovery in MDD patients. This blunted reactivity-impaired recovery pattern observed among the afternoon studies was most pronounced in studies with older and more severely depressed patients.

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Bruce McEwen (2003)

The brain controls both the physiologic and the behavioral coping responses to daily events as well as major stressors, and the nervous system is itself a target of the mediators of those responses through circulating hormones. The amygdala and hippocampus interpret what is stressful and regulate appropriate responses. The amygdala becomes hyperactive in posttraumatic stress disorder (PTSD) and depressive illness, and hypertrophy of amygdala nerve cells is reported after repeated stress in an animal model. The hippocampus expresses adrenal steroid receptors. It undergoes atrophy in several psychiatric disorders and responds to repeated stressors with decreased dendritic branching and reduction in number of neurons in the dentate gyrus. Stress promotes adaptation ("allostasis"), but a perturbed diurnal rhythm or failed shutoff of mediators after stress ("allostatic state") leads, over time, to wear and tear on the body ("allostatic load"). Neural changes mirror the pattern seen in the cardiovascular, metabolic, and immune systems, that is, short-term adaptation versus long-term damage. Allostatic load leads to impaired immunity, atherosclerosis, obesity, bone demineralization, and atrophy of nerve cells in brain. Allostatic load is seen in major depressive illness and may also be expressed in other chronic anxiety disorders such as PTSD and should be documented.

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Author and article information

Journal

Journal ID (nlm-ta): Braz J Med Biol Res

Journal ID (iso-abbrev): Braz. J. Med. Biol. Res

Journal ID (publisher-id): bjmbr

Title: Brazilian Journal of Medical and Biological Research

Publisher: Associação Brasileira de Divulgação Científica

ISSN (Print): 0100-879X

ISSN (Electronic): 1414-431X

Publication date (Electronic): 06 February 2017

Publication date Collection: 2017

Volume: 50

Issue: 2

Electronic Location Identifier: e5577

Affiliations

[1 ]Department of Otorhinolaryngology, School of Medicine, University of Medicine and Pharmacy “Grigore T. Popa”, Iasi, Romania

[2 ]Department of Internal Medicine, School of Medicine, University of Medicine and Pharmacy “Grigore T. Popa”, Iasi, Romania

[3 ]Department of Pharmacology, School of Medicine, University of Medicine and Pharmacy “Grigore T. Popa”, Iasi, Romania

[4 ]Department of Psychology, Sapienza University of Rome, Rome, Italy

[5 ]Department of Physiology and Pharmacology “V. Erspamer”, Sapienza University of Rome, Rome, Italy

Author notes

Correspondence: F.R. Patacchioli: francesca.patacchioli@ 123456uniroma1.it

[*]

These authors contributed equally to this study.

Article

Other ID: 00201

DOI: 10.1590/1414-431X20165577

PMC ID: 5390531

PubMed ID: 28177057

SO-VID: ee829968-0aa6-4e79-b73d-03638c9c1d8e

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 8 June 2016

Date accepted : 23 November 2016

Page count

Figures: 1, Tables: 1, Equations: 0, References: 88, Pages: 1

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