Chronic stress exposure decreases the cortisol awakening response in healthy young men

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Abstract

Academic examination is a major stressor for students in China. Investigation of stress-sensitive endocrine responses to major examination stress serves as a good model of naturalistic chronic psychological stress in an otherwise healthy population. The cortisol awakening response (CAR) is an endocrine marker of the hypothalamic-pituitary-adrenocortical (HPA) axis in response to stress. However, it remains unknown how chronic examination stress impacts the CAR in a young healthy population To exclude the influence of sex effects on hormone level, the CAR and psychological stress responses were assessed on two consecutive workdays in 42 male participants during their preparations for the Chinese National Postgraduate Entrance Exam (NPEE) and 21 non-exam, age-matched male comparisons. On each day, four saliva samples were collected immediately after awakening, 15 minutes, 30 minutes and 60 minutes after awakening. The waking level (S1), the increase within 30 minutes after awakening (R30), the area under the curve with respect to ground (AUCg), and the area under the curve with respect to increase (AUCi) were used to quantify the CAR. Psychological stress and anxiety were assessed by the Perceived Stress Scale and the Spielberger State-Trait Anxiety Inventory, respectively. Male participants in the exam group had greater perceived stress and anxiety scores relatibe to the non-exam group. Both R30 and AUCi in the exam group were significantly lower than the comparison group and this effect was most pronounced for participants with high levels of perceived stress in the exam group. Perceived stress and anxiety levels were negatively correlated with both R30 and AUCi. Chronic examination stress can lead to the decrease of CAR in healthy young men, possibly due to reduced HPA axis activity under long-term sustained stress.

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A new view on hypocortisolism.

Eva Fries, Judith Hesse, Juliane Hellhammer … (2005)

Low cortisol levels have been observed in patients with different stress-related disorders such as chronic fatigue syndrome, fibromyalgia, and post-traumatic stress disorder. Data suggest that these disorders are characterized by a symptom triad of enhanced stress sensitivity, pain, and fatigue. This overview will present data on the development, mechanisms and consequences of hypocortisolism on different bodily systems. We propose that the phenomenon of hypocortisolism may occur after a prolonged period of hyperactivity of the hypothalamic-pituitary-adrenal axis due to chronic stress as illustrated in an animal model. Further evidence suggests that despite symptoms such as pain, fatigue and high stress sensitivity, hypocortisolism may also have beneficial effects on the organism. This assumption will be underlined by some studies suggesting protective effects of hypocortisolism for the individual.

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Psychosocial stress reversibly disrupts prefrontal processing and attentional control.

C Liston, B S McEwen, B. J. Casey (2009)

Relatively little is known about the long-term neurobiological sequelae of chronic stress, which predisposes susceptible patients to neuropsychiatric conditions affecting the prefrontal cortex (PFC). Animal models and human neuroimaging experiments provide complementary insights, yet efforts to integrate the two are often complicated by limitations inherent in drawing comparisons between unrelated studies with disparate designs. Translating from a rodent model of chronic stress where we have shown reversible disruption of PFC function, we show that psychosocial stress induces long-lasting but reversible impairments in behavioral and functional magnetic resonance imaging (fMRI) measures of PFC function in humans. Twenty healthy adults, exposed to 1 month of psychosocial stress, confirmed by a validated rating scale, were scanned while performing a PFC-dependent attention-shifting task. One month later, they returned for a second scanning session after a period of reduced stress, and their performance was compared with a twice-scanned, matched group of low-stress controls. Psychosocial stress selectively impaired attentional control and disrupted functional connectivity within a frontoparietal network that mediates attention shifts. These effects were reversible: after one month of reduced stress, the same subjects showed no significant differences from controls. These results highlight the plasticity of PFC networks in healthy human subjects and suggest one mechanism by which disrupted plasticity may contribute to cognitive impairments characteristic of stress-related neuropsychiatric conditions in susceptible individuals.