High cortisol responders to stress show increased sedation to alcohol compared to low cortisol responders: An alcohol dose-response study.

AIMS: The present study was designed to examine the relationship between high and low cortisol response to an acute stressful situation and the subjective effects after different doses of alcohol, in healthy social drinkers. METHOD: Sixty-four subjects (32 men and 32 women) participated in one laboratory session. They performed a modified version of the Trier Social Stress Test (TSST) immediately before consumption of either placebo or alcohol (0.2, 0.4 or 0.8 g/kg). Subjects in each dose group were then divided into high (HCR; n=32) or low (LCR; n=32) cortisol responders. Primary dependent measures were self-report questionnaires of mood. RESULTS: The HCR reported increased ratings on Sedation on the Biphasic Alcohol Effects Scale (BAES) with increased dose in comparison with the LCR. This increase in sedation also correlated to the increase in cortisol levels. CONCLUSION: We conclude that a high cortisol response to stress modulates the subjective response to alcohol, dose-dependently. HCR subjects experience increased sedative effects of alcohol after consumption of higher doses of alcohol following stress compared to LCR subjects.

A family history of Type 1 alcoholism differentiates alcohol consumption in high cortisol responders to stress.

BACKGROUND: The differentiation between high and low cortisol responders to stress is of interest in determining the risk factors which may, along with genetic vulnerability, influence alcohol intake. METHODS: Thirty-two healthy volunteers, family history positive to alcoholism (FHP, n = 16) and family history negative (FHN, n = 16) attended two laboratory sessions during which alcohol or placebo was offered. RESULTS: There were no differences in consumption of alcohol or placebo between FHP and FHN subjects. STUDY 2: METHODS: Fifty-eight healthy social drinkers, FHP (n = 27) and FHN (n = 31) attended two laboratory sessions. They were administered either alcohol or placebo in both sessions they attended. All subjects underwent either a stress task (the Trier Social Stress Test, TSST) or a stress-free period, at two separate occasions, before being offered beverage. After the salivary cortisol analysis, subjects in each group were divided into high (HCR) or low (LCR) cortisol responders. RESULTS: After stress, subjects who were FHP-HCR consumed more alcohol than FHN-HCR. There were no differences in the placebo intake between FHP and FHN subjects regardless of their cortisol response. CONCLUSIONS: This result indicates that stress promotes alcohol consumption only in subjects with a family history of Type 1 alcoholism who show an increase in cortisol response to stress. This behaviour is similar to that previously observed in alcohol dependent individuals after stress and thus could represent an endophenotype posing a risk for future development of alcohol use disorders.

Stress and consumption of alcohol in humans with a Type 1 family history of alcoholism in an experimental laboratory setting.

BACKGROUND: This paper investigates how stress interacts with alcohol consumption in subjects with a family history of alcoholism. One mechanism for increases in alcohol intake may be that stress alters the subjective effects produced by the drug. METHODS: 58 healthy volunteers, divided into two groups of family history positive (FHP) and two groups of family history negative (FHN) participated in two laboratory sessions, in which they performed in one out of two sessions a stress task. Then subjects were allowed to choose up to six additional drinks of ethanol or placebo depending on which session they were randomly assigned to start with. RESULTS: It was found that FHP subjects increased their consumption of alcohol after stress. CONCLUSIONS: It is possible that both stress and alcohol specifically exaggerate the feelings of the reward in the FHP individuals in such way that it may increase the likelihood of consuming more alcohol.