Bernhard Croissant1, Robert Olbrich. 1. Central Institute of Mental Health, J5, D-68159 Mannheim, Germany. croissant@zi-mannheim.de
Abstract
OBJECTIVE: This study examines the stress-response-dampening (SRD) hypothesis of alcoholism from a novel vantage point. Various investigators have demonstrated that persons considered to be at risk for developing alcohol-related problems exhibit attenuation of stress reactions in psychologically challenging experimental sessions after receiving alcohol. These studies have used autonomic nervous system measures for indexing stress responses. In our report we address the question of whether people with a family history of alcoholism exhibit dampening effects of ethanol in the response of a classical stress hormone (i.e., cortisol). METHOD: Subjects in this report were 46 healthy male and 40 healthy female adult subjects; 36 of the men were sons and 28 of the women were daughters of alcohol-dependent fathers (sons of alcoholics, SOAs; daughters of alcoholics, DOAs); 12 women and 10 men had no family history of any alcohol use disorders (daughters of nonalcoholics, DONAs; sons of nonalcoholics, SONAs). The subjects were part of a large-scale project in which participants received two laboratory sessions with exposure in each to three experimental paradigms involving psychological stress while various psychophysiological and neuroendocrine measures were taken. In one of the sessions alcohol was administered. RESULTS: In the 1-hour period after termination of the stress paradigms, SOAs showed significantly lower plasma cortisol levels on laboratory days with alcohol administration than on days without alcohol administration at two of the three poststress sampling points. DOAs, however, did not exhibit a dampening pattern for cortisol. In the two control groups of SONAs and DONAs, no stress response attenuation effects of alcohol were observed. CONCLUSIONS: The results of experimental laboratory work with individuals at risk of alcoholism in the present and other studies add to the validity of SRD models of this disorder. Research strategies that should provide direct evidence for the SRD hypothesis are addressed in the Discussion section.
OBJECTIVE: This study examines the stress-response-dampening (SRD) hypothesis of alcoholism from a novel vantage point. Various investigators have demonstrated that persons considered to be at risk for developing alcohol-related problems exhibit attenuation of stress reactions in psychologically challenging experimental sessions after receiving alcohol. These studies have used autonomic nervous system measures for indexing stress responses. In our report we address the question of whether people with a family history of alcoholism exhibit dampening effects of ethanol in the response of a classical stress hormone (i.e., cortisol). METHOD: Subjects in this report were 46 healthy male and 40 healthy female adult subjects; 36 of the men were sons and 28 of the women were daughters of alcohol-dependent fathers (sons of alcoholics, SOAs; daughters of alcoholics, DOAs); 12 women and 10 men had no family history of any alcohol use disorders (daughters of nonalcoholics, DONAs; sons of nonalcoholics, SONAs). The subjects were part of a large-scale project in which participants received two laboratory sessions with exposure in each to three experimental paradigms involving psychological stress while various psychophysiological and neuroendocrine measures were taken. In one of the sessions alcohol was administered. RESULTS: In the 1-hour period after termination of the stress paradigms, SOAs showed significantly lower plasma cortisol levels on laboratory days with alcohol administration than on days without alcohol administration at two of the three poststress sampling points. DOAs, however, did not exhibit a dampening pattern for cortisol. In the two control groups of SONAs and DONAs, no stress response attenuation effects of alcohol were observed. CONCLUSIONS: The results of experimental laboratory work with individuals at risk of alcoholism in the present and other studies add to the validity of SRD models of this disorder. Research strategies that should provide direct evidence for the SRD hypothesis are addressed in the Discussion section.