Beatrice A. Rouse
University of North Carolina at Chapel Hill
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Annals of the New York Academy of Sciences | 1976
John A. Ewing; Beatrice A. Rouse; Robert A. Mueller; Kenneth C. Mills
Although alcohol is almost certainly the drug in longest use and although the ethanol molecule is a relatively simple one, the effects of alcohol upon living organisms are enormously complex. For the most complex organism, man, we know remarkably little about how alcohol produces its effects. Ethanol has long been known to be a general depressant of activity in all living cells.’ However, a naive observer of a cocktail party. as he noticed the increasing euphoria and general uproariousness of the participants, would find it difficult to accept that this is the behavior of depressed people, or at least that of people with depressed central nervous systems (CNS). Thus, it is not surprising that lay people often label alcohol as a “stimulant.” Of course, the standard medical explanation for this phenomenon is disinhibition: alcohol, like other CNS depressants, first affects. the phylogenetically newer parts of the brain. those concerned with self-evaluation and control, particularly in the social setting. By selectively depressing or inhibiting such centers, alcohol appears to promote the release of behavior that otherwise would be suppressed.? However, there is increasing interest in the possibility that alcohol can produce direct stimulation effects, including euphoria in man. A major issue that remains to be elucidated is the relative role of acetaldehyde, the first metabolic breakdown product of alcohol.3 This highly reactive substance appears to be significantly more toxic than alcohol itself.4 Evidence suggests that certain organisms may metabolize acetaldehyde less efficiently than others, thus possibly being subject to more of the effects of acetaldehyde, whatever they may be.s Also, although earlier studies found no difference in blood acetaldehyde levels in alcoholics and n o n a l c o h ~ l i c s , ~ ~ ~ Korsten et al. recently reported data that showed higher levels in alcoholics that did not merely represent more rapid metabolism.” Thus, this subject must be studied in more detail.
American Journal of Psychiatry | 1974
John A. Ewing; Beatrice A. Rouse; E. D. Pellizzari
Addiction | 1976
John A. Ewing; Beatrice A. Rouse
American Journal of Psychiatry | 1971
Martin H. Keeler; John A. Ewing; Beatrice A. Rouse
American Journal of Psychiatry | 1973
John A. Ewing; Beatrice A. Rouse
American Journal of Psychiatry | 1977
John A. Ewing; Mueller Ra; Beatrice A. Rouse; Silver D
American Journal of Psychiatry | 1973
Beatrice A. Rouse; John A. Ewing
Alcoholism: Clinical and Experimental Research | 1978
John A. Ewing; Beatrice A. Rouse; Robert A. Mueller; David Silver
Alcoholism: Clinical and Experimental Research | 1980
John A. Ewing; Beatrice A. Rouse
American Journal of Psychiatry | 1972
Beatrice A. Rouse; John A. Ewing