Part of this work was presented in the First International Symposium on Alcohol and Aldehyde Metabolizing Systems in Stockholm, July 1973.
Metabolic Studies on the Pathogenesis of Hangover
Article first published online: 28 JUN 2008
European Journal of Clinical Investigation
Volume 4, Issue 1, pages 93–100, February 1974
How to Cite
Ylikahri, R. H., Huttunen, M. O., Eriksson, C. J. P. and Nikklä, E. A. (1974), Metabolic Studies on the Pathogenesis of Hangover. European Journal of Clinical Investigation, 4: 93–100. doi: 10.1111/j.1365-2362.1974.tb00378.x
- Issue published online: 28 JUN 2008
- Article first published online: 28 JUN 2008
- Received: July 26, 1973, and in revised form: November 27, 1973
- free fatty acids;
Abstract. A variety of metabolic parameters were evaluated in 23 healthy male volunteers, after ethanol administration (1.5 g/kg) and correlated to the symptoms of hangover. The degree of intoxication and hangover were estimated using a simple test program according to which 11 subjects had severe and 12 mild hangover. Sequential determinations of blood ethanol, acetaldehyde, glucose, lactate, free fatty acids (FFA), triglycerides (TG) and ketone bodies were made during the 21 hours after administration. Each subject served as his own control by taking part in an identical experimental session but receiving no ethanol.
The maximal hangover occurred 12 to 14 hours after the initiation of drinking. At this time almost all of the ethanol and acetaldehyde had been eliminated from the blood. The intensity of the hangover did not correlate with the peak concentrations of ethanol or acetaldehyde in the blood. Marked hypoglycemia regularly followed the administration of ethanol, but the nadir blood glucose values had no correlation with the intensity of hangover. Ethanol induced a significant rise in blood lactate concentration, the extent of which was similar in subjects with mild or severe hangover.
During the most intensive hangover plasma FFA level increased when compared to the values observed during the control period. These concentrations were significantly higher in subjects with severe hangover than in those whose hangover was mild. An increase in plasma TG concentration regularly followed ethanol administration but the extent of the rise did not correlate with the degree of intoxication or hangover. Ethanol had a marked antiketogenic effect during the first 8 hours of the experiment after which the concentration of ketone bodies rose rapidly above the control level. Again the changes showed no correlation with the intensity of hangover.
The results indicate that the intensity of hangover bears little relation to the changes in the metabolite concentrations measured. This suggests that the symptoms of hangover can not be accounted for by the ethanol-induced alterations of the major blood metabolite concentrations.