One can see that the human body contains a very sophisticated series of mechanisms that have evolved to enhance survival. When stressors and the subsequent physiological changes that are adaptive in the short run are chronic, however, they may produce long-term health risks. This idea was first discussed in detail in the mid-twentieth century by physiologist Hans Selye, who coined the term "general adaptation syndrome" to describe the body's physiological responses to stressors and the mechanisms by which these responses might result in disease.
Selye's general adaptation syndrome involves three stages of physiological response: alarm, resistance, and exhaustion. During the alarm stage, the organism detects a stressor and responds with SNS and hormonal activation. The second stage, resistance, is characterized by the body's efforts to neutralize the effects of the stressor. Such attempts are meant to return the body to a state of homeostasis, or balance. (The concept of homeostasis, or the tendency of the body to seek to achieve an optimal, adaptive level of activity, was developed earlier by Walter Cannon.) Finally, if the resistance stage is prolonged, exhaustion occurs, which can result in illness. Selye referred to such illnesses as diseases of adaptation. In this category of diseases, he included hypertension, cardiovascular disease, kidney disease, peptic ulcer, hyperthyroidism, and asthma.
Selye's general adaptation syndrome has received considerable attention as a useful framework within which to study the effects of stressors on health, but there are several problems with his theory. First, it assumes that all stressors produce characteristic, widespread physiological changes that differ only in intensity and duration. There is compelling evidence, however, that different types of stressors can produce very different patterns of neural and hormonal responses. For example, some stressors produce increases in heart rate, while others can actually cause heart rate deceleration. Thus, Selye's assumption of a nonspecific stress response must be questioned.
Also, Selye's theory does not take into account individual differences in the pattern of response to threat. Research during the later twentieth century demonstrated that there is considerable variability across individuals in their physiological responses to identical stressors. Such differences may result from genetic or environmental influences. For example, some studies have demonstrated that normotensive offspring of hypertensive parents are more cardiovascularly responsive to brief stressors than individuals with normotensive parents. Although one might conclude that the genes responsible for hypertension have been passed on from the hypertensive parents, these children might also have different socialization or learning histories that contribute to their exaggerated cardiovascular reactivity to stressors. Whatever the mechanism, this research highlights the point that individuals vary in the degree to which they respond to stress and in the degree to which any one organ system responds.
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