Earlier accounts of allostasis overlooked our evolutionary context. When in our evolutionary past have we had prolonged periods of restfulness (Wingfield and Ramenofsky, 1997; Wingfield and Romero, 2001)? We need to take evolution into account as we consider homeostasis, stress, allostasis, and allostatic overload. For example, high levels of corticosterone can favor or support animals in a wide variety of contexts; in a number of species, levels of corticosterone or cortisol can be adjusted in the short term by both behavioral and physiological means (Wing-field and Ramenofsky, 1997). In the short term, glucocorticoids are protective and facilitate normal physiological and behavioral adaptation. But in the long run, high levels of corticosterone interfere with a number of regulatory functions (McEwen, 1998a, b, 2000).
Constant stimulation is not new; our increasing life expectancy is. Tissue declines with age. Rousseau (1762) asked the question, "Why are men in chains when they are born free?" Perhaps an analogous question is, Why is there so much worry when we have so much? One reason is that if we don't find worry, we are very good at constructing it. This is not just a piece of pathology.
The dominant theme that led to the concept of allostasis is that chronic arousal of the brain drives increases in regulatory physiology to a point beyond what is acceptable for normal function. Evolution favored a number of specialized mechanisms in the brain in regulating both behavioral and physiological functions. When activated inappropriately, normal maintenance turns into pathological vulnerability and expression (figure C.4).
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