Abstract
Purpose of ReviewThis review focuses on the concentration of cortisol in human hair as a biomarker of chronic stress in cardiovascular disease (CVD). We outline the cardiovascular consequences of cortisol excess and provide a comprehensive overview of recent studies investigating the relationship of hair cortisol with CVD. In addition, clinical implications and limitations of the evidence are discussed, together with directions for future research.Recent FindingsHair cortisol may be a reliable biomarker of chronic stress since it provides quantification of total cortisol secreted into hair over several weeks. A growing body of evidence suggests that elevated hair cortisol levels are associated with both the incidence of CVD and poorer recovery and treatment outcomes. Moreover, increased hair cortisol concentration has been linked with established cardiometabolic risk factors for CVD including high blood pressure, diabetes, and adiposity.SummaryHair cortisol is a promising biomarker of chronic cortisol excess which may contribute to both the pathogenesis and prognosis of CVD. However, the current evidence relies on small-scale cross-sectional studies. Further research adopting longitudinal designs across larger samples of CVD patients and healthy participants is required to inform the development of novel evidence-based interventions.
Highlights
Cardiovascular disease (CVD) is a leading contributor to the burden of morbidity and mortality across the world
This review focuses on the role of hair cortisol as a biomarker of chronic stress in CVD
Given the elevated CVD risk observed in patients with Cushing’s syndrome and those treated with glucocorticoid therapy, several studies have investigated the relationship of endogenous cortisol levels with the development and progression of CVD in both clinical and population-based samples
Summary
Cardiovascular disease (CVD) is a leading contributor to the burden of morbidity and mortality across the world. Acute and transient HPA-axis activation has an adaptive function since it facilitates effective coping with external stressors by triggering a number of physiological reactions. These include, for instance, increased vascular tone, immune activation, suppression of inflammation, energy mobilisation, insulin resistance, inhibition of reproductive physiology and behaviour and sharpened cognition [30]. Increased adiposity contributes to other CVD risk factors since fat cells release hormones and metabolites that adversely affect blood pressure, plasma lipoproteins, coagulation and insulin resistance [29]. Patients treated with high doses of glucocorticoids have been shown to have substantially higher risk of cardiovascular events and adverse cardiometabolic markers [32, 36]
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