Cortisol and Stress

Cortisol and the HPA Axis System

Cortisol circulates at basal levels to keep the body at a balanced level but becomes elevated in response to stress (Stansbury & Gunnar, 1994). Often, this process is referred to as emotion regulation strategies (Nachmias, Gunnar, Mangelsdorf, Parritz, & Buss, 1996). Emotion regulation strategies serve an important function in stress resistance because of their involvement with the mobilization of resources necessary for action in response to stress.

Stress reactivity and adaptation is managed by the hypothalamic-pituitary-adrenal (HPA) axis system (Sapolsky, 1992). When the system experiences stress, [Page 298]within minutes, the corticotrophin-releasing hormone (CHR) is released from the hypothalamus and travels to the pituitary (Brown, 2000). Once it arrives at the pituitary, it stimulates the release of andrenocorticotropic hormone (ACTH). ACTH is quickly released into the general circulation. When it reaches the adrenal glands, ACTH stimulates the production and release of cortisol. This process of hormone release is known as the stress response (Brown, 2000).

The HPA system is regulated in part via central glucocorticoid negative feedback. This occurs because cortisol is a steroid hormone and is allowed to freely cross the blood-brain barrier. Circulating cortisol is able to regulate its own production and release by inhibiting the production of CHR and ACTH (Sapolsky, 1992). In effect, cortisol is the primary means of regulating the HPA response to stress and is the end product of this process; as a result, researchers use it as a marker.

Psychological Risks of Elevated Cortisol Levels

While short-term elevated cortisol levels can be crucial in preparing humans for danger, elevated cortisol levels that occur over an extended period of time can have a detrimental effect on the body. Individuals suffering from prolonged exposure to cortisol may also be at heightened risk for a variety of negative health problems, including depression, hippocampal atrophy, cognitive impairment, abdominal obesity, postpartum stress, and loss of bone density (Brown, Varghese, & McEwen, 2004).

Various studies have shown that one of the possible effects of long-term cortisol exposure is damage to the area of the brain that is involved with learning and memory (Sapolsky, 1985). Coe, Rosenberg, and Levine (1988) found that sustained, elevated cortisol levels can result in impaired immune functioning. Therefore, it is important to study the mechanisms that influence cortisol, to help prevent negative physiological outcomes.

Recent studies have found an interaction between stressful events and vulnerability for depression (Heim & Nemeroff, 1999). This interaction may have a crucial role in the onset of depression. The biological abnormalities that are most often found in depressed individuals involve deviations in hypothalamic-pituitary-adrenal axis functioning (Sapolsky, 1992). About half of patients with depression exhibit elevated cortisol levels (Brown et al., 2004).

There are overlapping medical problems exhibited by individuals with Cushing's disease and individuals with depression. Cushing's disease is an illness characterized by ACTH-secreting pituitary tumors. As a result of the pituitary tumors, this illness has been associated with cortisol elevation. These commonalities in medical illnesses have provided evidence of the detrimental effects of elevated cortisol (Brown et al., 2004).

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