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AN EXTENSION OF THE STRESS-HOMEOSTASIS MODEL BASED ON ETHOLOGICAL RESEARCH GLENNE. WEISFELD* Introduction The concept of stress, and specifically the General Adaptation Syndrome (GAS), was originally a physiological notion. It carries great explanatory power on this level, embracing as it does a panoply of adjustments to a variety ofenvironmental stimuli, or stressors. This level of explanation is referred to by biologists asproximate causation, the operation of environmental and physiological causal factors. Similarly, the recent concept of stress as psychological [1] focuses on this mechanistic level, psychological factors being posited as intervening between stressor and physiological changes. The other level of biological explanation is ultimate causation, which concerns evolutionary function. Physiological systems and behavior patterns presumably evolved to promote the organism 's survival and reproduction and hence are adaptive. These two levels of understanding are interrelated, since they constitute different perspectives on the same evolved phenomena. A complete understanding of a biological phenomenon—morphological, physiological, or behavioral—requires comprehension on both levels. We are not fully satisfied with learning how a bodily system works in mechanical terms; we also want to know why it evolved, what functional value it has. Being an applied science, medicine naturally has concentrated on proximate explanations, especially of pathological processes. From this perspective it is easy to lose sight of normal functioning and particularly its adaptive, or ultimate, causation. Yet a full appreciation of nature's designs may be of great practical value in guiding the development and appreciation of interventive techniques. Biological systems that are relatively well understood, such as hemodynamics and the visual system, are The generous and valuable assistance of Drs. Glenn Elliott, Martha K. McClintock, Alice M. Young, and Vicki Weisfeld is gratefully acknowledged. ?Department of Psychology, Wayne State University, Detroit, Michigan 48202.© 1982 by The University of Chicago. All rights reserved. 0031-5982/83/2601-0291$01.00 Perspectives in Biology and Mediane, 26, 1 ¦ Autumn 1982 | 79 comprehended in adaptive, even aesthetic, terms, as well as on the purely mechanistic level. This essay is an attempt to extend the stress concept along functional, or adaptive, lines. Initial Extension of the Stress-Homeostasis Model Adaptation is the GAS's middle name, and yet these bodily adjustments may not be fully appreciated in evolutionary terms. The bodily adjustments to stressors must necessarily be part of an evolved, adaptive system, but since these adjustments often give rise to pathological changes, the "wisdom of the body" can be overlooked. The term GAS refers to adaptation in the psychological sense of adjustment to a stimulus, rather than to the biological concept of an evolved change in response to a selection pressure. The problem of viewing these bodily adjustments functionally is probably aggravated by use of the terms "stress," which sounds pathological, and "stage of exhaustion," which suggests that the body ultimately adjusts itself to death. In reality, most cases ofdeath probably occur despite the organism's compensatory processes rather than because of them. Actual demonstrations of the stage of exhaustion in normal organisms are dubious [2], but, even if they do commonly occur, the body's evolved mechanisms for compensation can hardly be blamed for demise in the face of unrelenting insult. The GAS, then, can probably be better appreciated in terms of its adaptiveness. Toward this end, let us first review the widespread bodily ramifications of exposure to a stressor. Stressors increase adrenal corticosteroid production, which raises blood glucose and free fatty acid levels and stimulates the CNS. The corticosteroids also increase salt and hence fluid retention, speed clotting time, and raise blood pressure. These changes offer protection in a stressful situation that threatens the organism with fluid loss through hemorrhage or profuse sweating. This "stage of resistance" is complemented by the "flight-fight" adrenomedullary sympathetic discharge pattern described by Cannon [3]. Under similar stressful conditions, the sympathetic division releases catecholamines, which increase heart rate and. contractility, raise blood pressure, increase respiration, arouse the CNS, raise blood glucose and free fatty acid levels, decrease muscle fatigue, release RBCs from the spleen, speed coagulation, stimulate the erectores pili,1 and divert blood from skin to muscles. AU of these adjustments would be adaptive for an organism whose life was threatened by trauma. Furthermore, the...


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