By George S. Everly Jr.
This new version emphasizes the original contribution of this longstanding text within the integration of mind/body relationships. the concept that of rigidity, as outlined and elaborated in bankruptcy 1, the first efferent organic mechanisms of the human tension reaction, as defined in bankruptcy 2, and the hyperlink from pressure arousal to affliction, as outlined in bankruptcy three, primarily is still an identical. although, updates in microanatomy, biochemistry and tomography are additional to those chapters. All different chapters could be up-to-date besides, as there was major adjustments within the box during the last 8 years.
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Extra info for A Clinical Guide to the Treatment of the Human Stress Response
The Effects of the Glucocorticoid Hormones a and HPAC Activation Increased glucose production (gluconeogenesis) Exacerbation of gastric irritation Increased urea production Increased release of free fatty acids into systemic circulation Increased susceptibility arteherosclerotic processes Increased susceptibility to nonthrombotic myocardial necrosis Thymicolymphatic atrophy (demonstrated in animals only) Supression of immune mechanisms Exacerbation of herpes simplex Increased ketone body production Appetite supression Associated feelings of depression, hopelessness, helplessness, and a loss of control aSee Henry & Stephens (1977), Selye (1976), Yates & Maran (1972), Yuwiler (1976), MaCabe & Schneiderman (1984), Makara, Palkovitz, & Szentagothal (1980) for reviews.
As the prepotent mineralocorticoid, aldosterone may effect other physiologic outcomes, among them increasing glycogen deposits in the liver and decreasing circulating eosinophils. Excessive activation of mineralocorticoid secretion in human beings has been implicated in the development of Cushing's syndrome (hyperadrenocorticism) by Gifford and Gunderson (1970) and in high blood pressure and myocardial necrosis by Selye (1976). As a tropic hormone, the main function of ACTH is to stimulate the synthesis and secretion of the glucocorticoid hormones from the adrenal cortex, yet ACTH is known to cause the release of cortical adrenal androgenic hormones such as testosterone as well.
Perhaps clearest of all is the fact that each sympathetic and parasympathetic effect is not manifest to all stressors. Therefore, what determines which stress-response mechanisms will be activated by which stressors in which individuals? The answer to this question is currently unknown. However, there is some evidence to suggest the existence of a psychophysiological predisposition for some individuals to undergo stressresponse pattern specificity (see Sternbach, 1966). We will expand on this topic in Chapter 3.