Differences in the Peripheral Levels of β‐endorphin in Response to Alcohol and Stress as a Function of Alcohol Dependence and Family History of Alcoholism

: Background: Evidence indicates that both genetic and environmental factors, such as stress, may play an important role for the development of alcoholism, while β-endorphin may be implicated in the control of alcohol consumption. The objective of the present studies was to test the hypothesis that there are differences in the response of the pituitary β-endorphin system to stress as a function of family history of alcoholism and alcohol dependence. Methods: The response of the pituitary β-endorphin to a placebo or an alcohol (0.50g ethanol/kg) drink and to a stress task performed 30 min following ingestion of either the placebo or the alcohol drink was measured in social and heavy drinkers with [high risk (HR)] and without [low risk (LR)] a family history of alcoholism. Thus, each subject participated in 4 experimental sessions given on different days in a randomized order. Four groups of subjects were investigated: 1) low risk nonalcoholics (LRNA); 2) high risk nonalcoholics (HRNA), 3) low risk alcoholics (LRA); and 4) high risk alcoholics (HRA). Plasma β-endorphin was estimated prior to and for 3.5 hr post-stress. Changes in the concentration of plasma β-endorphin following ingestion of either the placebo or alcohol drink without performance of the stress task served as controls to compare the stress-induced changes. Results: Basal plasma β-endorphin levels were higher in LRNA than LRA, HRNA and HRA participants, while basal plasma β-endorphin levels were higher in LRA than those in HRNA and HRA participants. Furthermore, there was no significant difference in the plasma β-endorphin levels between HRNA and HRA participants. Stress, induced a significant increase in plasma β-endorphin concentration in all four groups of participants. However, the stress-induced increase in plasma β-endorphin levels was more pronounced in LRNA than HRNA, LRA and HRA participants. Thus, alcohol dependence decreased the basal plasma β-endorphin levels in LR only, as well as the stress induced increase in plasma β-endorphin levels of participants without, but not of those with, a family history of alcoholism. Alcohol prior to stress attenuated the stress-induced increase in plasma β-endorphin levels of all four groups of participants. Conclusions: The present data indicates that there are differences in both, the basal plasma β-endorphin levels as well as the response of the pituitary β-endorphin to stress as a function of family history of alcoholism and alcohol dependence. Thus, in HR individuals a dysfunction in the activity of the pituitary β-endorphin system predates the development of alcoholism, while in LR individuals it develops following alcohol dependence. Furthermore, alcohol dependence did not alter the alcohol-induced attenuation of β-endorphin response to stress.