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Salivary cortisol patterns in vital exhaustion
1Department of Psychiatry and Neuropsychology - PAR 45, Maastricht University, P.O. Box 616, 6200 MD, Maastricht, The Netherlands. n.nicolson@sp.unimaas.nl
Journal of Psychosomatic Research
|February 13, 2001
Summary
Vital exhaustion (VE), linked to heart attack risk, shows subtle hypothalamic-pituitary-adrenocortical (HPA) axis hypoactivity. Lower cortisol levels in VE patients correlate with fatigue and poor sleep, suggesting chronic stress impacts HPA function.
Area of Science:
- Endocrinology
- Psychoneuroimmunology
- Cardiovascular Disease Risk Factors
Background:
- Vital exhaustion (VE) is a syndrome of fatigue, irritability, and demoralization.
- VE is a recognized risk indicator for myocardial infarction.
- Hypothalamic-pituitary-adrenocortical (HPA) axis dysregulation is implicated in fatigue syndromes, but its role in VE is unclear.
Purpose of the Study:
- To investigate hypothalamic-pituitary-adrenocortical (HPA) axis function in men with vital exhaustion (VE).
- To assess basal free cortisol levels and cortisol reactivity to acute stress and morning awakening in VE patients compared to controls.
Main Methods:
- Salivary free cortisol was measured over two days in 29 VE men and 30 controls.
- Cortisol levels were assessed at basal state, in response to a speech task, and upon morning awakening.
- Perceived stress, sleep quality, and fatigue levels were also evaluated.
Main Results:
- VE subjects reported higher stress, poorer sleep, and greater fatigue.
- Basal cortisol levels were lower in VE subjects, particularly in the evening, and negatively correlated with fatigue.
- While overall cortisol responses to a speech task were similar, VE subjects showed fewer significant responses; awakening response correlated with fatigue and poor sleep.
Conclusions:
- Findings suggest subtle HPA axis hypoactivity in vital exhaustion.
- Chronic stress and associated sleep disturbances may contribute to this HPA hypoactivity in VE.
- This HPA axis dysfunction may be a mechanism linking VE to increased cardiovascular risk.
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