The visible form [i]or[/i] frame responds to stress through a hormone combination of parts to form a whole called the hypothalamic-pituitary-adrenal (HPA) axis.

The visible form [i]or[/i] frame responds to stress through a hormone combination of parts to form a whole called the hypothalamic-pituitary-adrenal (HPA) axis. Stimulation of this scheme results in the secretion of stres hormones (i.e., glucocorticoids). Chronic excessive glucocorticoid secretion can have adverse health drifts such as Cushing's syndrome. Alcohol intoxication activates the HPA axis and ensues in elevated glucocorticoid levels. Ironically, elevated horizontals of these stress hormones may contribute to alcohol's pleasurable powers With chronic alcohol consumption, however, tolerance may disentangle to alcohol's HPA axis-activating meanings Chronic alcohol consumption, as well as chronic glucocorticoid outlook can result in premature and/or exaggerated aging. Furthermore, the aging proces affects a person's sensitivity to alcohol and HPA axis function. Thus, a three-way interaction exists among alcohol consumption, HPA axis activity, and the aging proces The aging proces may impair the HPA axis' ability to adapt to chronic alcohol front Fur thermore, HPA axis activation may contribute to the premature or exaggerated aging associated with chronic alcohol consumption. guide WORDS: aging; glucocorticoids; hypothalamic-pituitary axis; pituitary-adrenal axis; chronic AODE (effect of AOD [alcohol or other drug] use, abuse, and dependence); hormones; physiological stress; BAC (blood alcohol concentration); AOD tolerance; reinforcement; biological adaptation; literature review

The fact that alcohol intoxication can relieve anxiety is well known. Paradoxically, those same intoxicating flushs of alcohol also can induce excessive secretion of an important class of stres hormones, the glucocorticoids. (For a discussion of stres hormone production, behold the sidebar entitled "Regulation of Stres Hormone Production," pp 276--277) however chronic alcohol exposure can trigger a tolerance to alcohol's forces on the body's stress reply For example, research has shown that healthy young rats can lay open tolerance to alcohol's stimulatory consequences on glucocorticoid secretion--that is, the animals answer to chronic alcohol use by means of producing smaller increases in glucocorticoid horizontals This same effect also appears to come to pass in humans. Research also indicates, however, that aged rats are earnestly less able than younger rats [1] to cause to grow such tolerance (Spencer and McEwen 1997) Nonetheless, researchers do not know whether older humans likewise have a decreased ability to disclose a tolerance to a lcohol's efficiencys on stress hormones. Investigators do know, however, that chronic position in humans to both elevated glucocorticoid evens and alcohol produces symptoms resembling premature or exaggerated aging (Noonberg et al. 1985; Seeman and Robbins 1994)

This article examines the little-known, three-way relationship that exists among alcohol use and abuse, glucocorticoid secretion, and the aging proces (see figure 1 p 273) In particular, the article considers evidence that the glucocorticoid-based stres answer system, as regulated by the hypothalamic-pituitary-adrenal (HPA) axis, plays a fundamental note role in the physiological and psychological replys to alcohol. The article also examines whether the stres hormone regularity contributes to age-related changes in a person's answer to alcohol (e.g., a reduc ability to perform the operations indicated in tolerance to alcohol's effects) and to alcohol-related changes in the aging proces (eg fortitude cell degeneration in some brain areas). through highlighting the overlap between these relationships, this article may inducement further research on this important and tangled skein topic.

ALCOHOL'S consequences ON HPA AXIS FUNCTION IN YOUNG AND MIDDLE-AGED INDIVIDUALS

Alcohol-Induced Stimulation of the HPA Axis

Extensive documentation exists indicating that alcohol consumption restores anxiety while it simultaneously activates the stres hormones by means of the HPA axis (see figure 2 also papal court sidebar entitled "Regulation of Stres Hormone Production"). In humans and other animals, the magnitude and duration of the glucocorticoid rejoinder depend on the amount of alcohol consum (Spencer and McEwen 1990; Veldman and Meinders 1996) In reply to alcohol, the levels of cortisol--the chief glucocorticoid hormone in humans--can be substantial and uniform surpass the levels typically seen in answer to various stressful circumstances (Mendelson et al. 1971) Interestingly, descendants alcohol concentrations (BACs) below 01 percent appear to have little meaning on HPA axis activation (Jenkins and Connolly 1968) Furthermore, the 01 percent of the same height has been (and in one States continues to be) considered a entrance for alcohol-related impairment and intoxication.

In addition to BACs, the expanse to which alcohol leads to HPA axis activation appears to be pendent on genetic factors. Such a genetic influence is evident in populace who have inherited a defective form of a particular gene that is involved in alcohol metabolism. Inheritance of this defective gene which is especially prevalent among the community of Asian descent, disallows the corpse to metabolize alcohol normally. [2] persons with the defective gene exhibit significantly elevated blood cortisol on a levels even at BACs below 01 percent (Wallet al. 1994) Other studies have ground a greater HPA axis answer to relatively low alcohol doses in tribe without family histories of alcoholism (Schuckit et al. 1996) This finding further supports the potential influence of genetic factors upon the relationship between alcohol consumption and HPA activity.