Stress and Adaptation

Regulation of adaptive responses is liable to lifelong modifications. The outcome of this developmental perspective of an individual is due to many factors including genetic background and aging per se but is also due to repeated environmental challenges (Fig. 12.1). Dealing with the stresses and strains of life, each individual reacts with a specific activation pattern of regulatory systems. In turn, this activation causes a secondary modification via a feedback reaction, thereby shaping specific response patterns depending on the point of time, frequency, duration, and power of the environmental

Figure 12.1. Possible interdependent links programming individual differences.

challenge. Therefore, every new environmental challenge causes a reaction, which depends on former experiences. In 1993, McEwen and Stellar defined allostasis as the process for adapting to environmental challenges to maintain homeostasis. Systems that vary according to demand, like the hypo-thalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system (ANS), actually help protect and maintain those systems that are truly homeostatic, (e.g., the blood pH or body temperature). Large variations in the HPA axis do not lead directly to death, as would large deviations in truly homeostatic systems. Therefore, McEwen and Stellar proposed that allostasis is the adequate term for physiological coping mechanisms. Examples of allostasis go to broader aspects of individual survival. In the immune system, an acute stress-induced release of catecholamines and glucocorti-coids facilitates the circulation and migration of immune cells to parts of the body where they are needed to fight an infection or to produce other immune responses (Dhabhar and McEwen, 1999). Furthermore, glucocor-ticoids and catecholamines act concertedly to promote the formation of memories of events of potentially dangerous situations so that the individual can avoid them in the future (Roozendaal, 2000). Yet, each of these adaptive processes has a potential cost to the body when allostasis is either called upon too often or is inefficiently managed, and that cost is referred to as allostatic load (McEwen and Stellar, 1993).

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