Stress has been shown to have an effect on the overall health of an individual (Chapman, Tuckett, & Song, 2008; Coe & Laudenslager, 2007). When unusual or social stressors are present, it can compound the already existing stress from a wound, resulting in a dysregulation of the supersystem, leading to a decline in health, function, and well-being. For example, a negative emotional state can have a large impact on the ability of wounds to heal quickly. This has profound implications for the individual’s ability to heal after surgery or trauma. Even such things as routine stress can have a negative impact on the ability of wounds to heal (Coe & Laudenslager, 2007). Moreover, exposure to acute psychological stress seems to trigger and increase in sympathetic adrenal activity, which in turn has an effect on the immune system (Kemeny & Schedlowski, 2007). In particular, Hypothalamic–Pituitary–Adrenal (HPA) axis-activity (which results in an increase in the release of glucocorticoids) and sympathetic mechanisms are the main mechanisms at work in the reduction or inhibition of cellular and humoral immune responses (Kemeny & Schedlowski, 2007).
The brain plays a major role in controlling the interpretation of what is stressful as well as the behavioral and physiological responses that are produced (Heuser & Lammers, 2003). Brief periods of controllable stress do not have a large impact on physical or mental health, however, when a person experiences a lack of control and uncertainty, a chronic state of distress can ensue, that increases vulnerability to stress-related disorders (Heuser & Lammers, 2003). In normal situations when stress is experienced by an individual, glucocorticoids are released from the adrenals to shut down the neural defensive reactions. A person in chronic stress can cause sustained increases in glucocorticoids, and in the case of humans, cortisol. When an individual overproduces stress hormones or is unable to terminate the activation of the HPA, maladaptive responses can occur. In certain cases, a chronic adaptation to a stressor can cause the HPA system to become tonically inhibited (Heuser & Lammers, 2003).
Stress affects the release of hormones which when overproduced can negatively affect the neuroendocrine response. Duncko, Makatsori, Fickova, Selko, and Jezova (2006) examined the relationship between high anxiety and impaired coordination of the stress response, global hyporesponsiveness, and hyperresponsiveness. It was hypothesized that high trait anxiety is correlated with impaired coordination of the stress response. The selection of volunteers was based on their score in the trait subtest of the State Trait Anxiety Inventory, and only subjects with scores higher than 45 and lower than 39 were included in the study. A total of 27 males were chosen for the study. 15 were placed into the anxious group and 12 in the non-anxious group based on scores. Anyone with a somatic or mental diseases, personal and/or family history of psychiatric disorders, body mass index higher than 28 and control blood pressure higher than 140/90 mmHg were excluded from the study. The subjects were asked to participate in a public speech. A spectrum of neuroendocrine parameters was measured before, during and after the speech. The results showed that high trait anxiety was correlated with as higher preference for emotion-oriented coping strategies but lower preference for task-oriented procedures. Additionally, high trait anxiety was correlated with lower scores on hardiness. The anxious group scored significantly higher in scales for stress, tiredness, arousal, anxiety and depression. Among the anxious group, a correlation was found between lower adrenocorticotropin (ACTH) and cortisol responses during stress, which was also correlated with an exaggerated perception of stress and worse mental performance. While this study is limited in only examining males and small sample size, this study provides more evidence that for those individuals susceptible and vulnerable to stress; neuroendocrine factors can play a role in fatigue, anxiety, depression, and inflammatory response (Duncko, Makatsori, Fickova, Selko, & Jezova, 2006).
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Chapman, C. R., Tuckett, R. P., & Song, C. W. (2008). Pain and stress in a systems perspective: Reciprocal neural, endocrine, and immune interactions. The Journal of Pain, 9(2), 122-145.
Coe, C. L., & Laudenslager, M. L. (2007). Psychosocial influences on immunity, including effects on immune maturation and senescence. Brain Behavior and Immunity, 21(8): 1000–1008. doi:10.1016/j.bbi.2007.06.015.
Duncko, R., Makatsori, A., Fickova, A., Selko, D., & Jezova, D. (2006). Altered coordination of the neuroendocrine response during psychosocial stress in subjects with high trait anxiety. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 30, 1058–1066.
Heuser , I & Lammers, C. (2003). Stress and the brain. Neurobiology of Aging 24, S69–S76.
Kemeny, M. E., & Schedlowski, M. (2007). Understanding the interaction between psychosocial stress and immune-related diseases: A stepwise progression. Brain, Behavior, and Immunity, 21, 1009-1018.