By definition, biopsychology stress may be defined as trauma or external condition that disturbs an individual’s psychological or physical well-being. Other authorities have defined stress as a reaction expressed by an individual to harm or threat. A number of stressors have been identified to cause psychological stress. These include; starvation, war, poverty, loss of a loved one, troubled relationships, heavy workloads and jobs involving high levels of responsibilities, a common factor in the western world. Psychological stress results in both mental or physical fear and depression. The immune system is also susceptible to advanced psychological stress leading to fungal or bacterial infections and stomach ulcers and gastritis, a condition referred to as inflammation. Psychological stress is categorized as short-term stress (adaptive) or long-term (maladaptive). Chronic psychological stress is clearly linked to major ill health described above. The brain and the system communicate with each other through a tiny protein referred to as neuropeptide Y that plays a dual role during periods when the body is under stress (Herzog, 2003). Neuropeptides are generated as a result of inflammatory response when the under stress. In his first description of stress, Selye identified a variety of psychological responses to stress giving much attention to the anterior pituitary-adrenal cortex system organs of the brain. He further concluded that all the common psychological stressors are associated with high levels of glucocorticoids, epinephrine and norepinephrine. The hippocampus has many glucocorticoid receptors which block the creation of new cells in the central nervous system which may lead to hippocampus cell damage observed in persons that are in advanced stages of depression. Following stress, the dendrites of pyramidal cells become shorter and less branched and adult neurogenesis of granule cells are reduced. The effects are blocked by adrenalectomy receptors produced in the corticosteroids. Studies have shown that natural stressors produce more pathological effects than artificial ones. However, effects are severe enough to disrupt behaviors mediated by the hippocampus organ. The second major brain structure affected by stress is the amygdala because it plays a major role in conditional fear. Fear is anxiety that disrupts normal functioning of the brain in most persons and is treated by benzodiazepines (Librium, Valium).
Auditory fear condition is blocked with medial geniculate nucleus (MGN) lesion. Amygdala contains high concentration of GABA receptors that blocks fear conditioning. In addition, amygdala and prefrontal cortex clearly play a role in brain mechanisms of human emotions. The strategies to regulate the immunity of stress may optimize the alleviation of stressful circumstances. For instance, epidemiological data show that social relationships are among the most crucial in person’s life. Situations threatening social factors are likely candidates to draw out suppression of immunity. Social networks have been suggested to act as a buffer against stress and require significant energy to be maintained. A number of authorities of research suggest that prolonged exposure to stress may lead to development of severe diseases in affected individuals (Black, 1995). Allostas model assumes that the person maintains function through environmental change. The person gradually responds to any stimuli that are risky with a pathway of changes. The individual affected will then calm down after the threatening period is over and the stress receptors are shut off. This kind of a mechanism that provides the physiological changes in response to stress is referred to as the allostatic load. A physiological process happens to change with response to environmental changes. On the other hand, the short-term response is highly adaptive in most persons. Persistent stress may lead to a variety of chronic diseases such as diabetes, coronary heart disease, and immune-related diseases (Black, 1995). The major role in this process is played by the hypothalamus-pituitary-adrenal (HPA). Although corticotrophin-releasing hormone and adrenocorticotropin (ACTH) also contribute to these disorders, the final product of this endocrine axis, cortisol, is suggested to be closely associated with majority of symptoms observed in stress associated health problems (Kirschbaum & Hellhammer, 1989). Inefficiency to achieve stability leads to cumulative negative effects (allostatic load) which is the price the body pays after being forced to adapt to psychological challenges and environments.
References
Black, H. (1995). Psychoneuroimmunology: brain and immunity. Science & Medicine, 2, 6-14. Herzog, H. (2003). Neuropeptide Y and energy homeostasis: Insights from Y receptor knockout models. European Journal of Pharmacology, 480 (1–3), 21–29.
Kirschbaum, C., & Hellhammer, D.H. (1989). Salivary cortisol in psychobiological research: an overview. Neuropsychobiology, 22, 150-169.