Although gross changes in personality and behavior are readily apparent during acute alcoholic intoxication, these changes have only become the subject of systematic study within the past 100 years. Miles (1932) has summarized the different stages of clinical intoxication in the form of a scale relating the subjective states and typical behavioral changes seen with increasing blood alcohol levels. The earliest effects, tingling sensations in the mucous membrane of the mouth and throat, may appear with a blood alcohol level as low as 10 mg%. At the upper extreme (300 mg%) the subject passes into a stuporous condition, and at still higher levels (400 mg%) falls into a state of deep anesthesia which may end in death. This description of successive stages in clinical intoxication represents the typical or modal response commonly seen with a given blood alcohol level. The association between blood alcohol concentration and stages of clinical intoxication is not a clear one-to-one relationship. As with other psychotropic drugs, there are large individual differences in response to a given dosage as well as considerable variability in the subject’s response at different times or in different settings.

Effects of high congener intake by human subjects on the EEG.

The Effects of Alcohol on the Central Nervous System in Humans

. 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 hypoglycaemia 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.

Metabolic studies on the pathogenesis of hangover

Ethyl alcohol is a potent pharmacologic agent with a wide variety of biochemical and neurophysiological effects, most marked in the central nervous system but by no means restricted to it The mechanisms of these pharmacological actions are not only poorly understood but are assumed to involve a wide spectrum of enzyme effects in addition to physiochemical effects on other parameters of drug activity such as membrane permeability, electrolyte activities, and so on Consequently, it is not surprising that ethyl alcohol should both affect the action of other drugs and be affected by them These interactions run the gamut from antagonistic effects with mutual neutralization to simple addition of similar effects to actual potentiating interactions where the total effect of the two drugs is greater than the sum of the effects of the two drugs alone The mechanisms of these interactions are even less well understood than those for the individual drugs The purpose of the chapter is to review those studies dealing with the empirical data describing the pharmacologic and behavorial effects of alcohol and drug combinations and also those studies which may illuminate the mechanisms of those interactions

Effects of high congener intake by human subjects on the EEG.

Citations

The Effects of Alcohol on the Central Nervous System in Humans

Metabolic studies on the pathogenesis of hangover

Interactions of Ethyl Alcohol and Other Drugs

The effects of ethanol on EEG activity in males at risk for alcoholism

Alcoholism, alpha production, and biofeedback.

Related Papers (3)

The effects of alcohol upon the electroencephalogram (brain waves).

Experimental induction of hangover.

The appearance of some congeners of alcoholic beverages and their metabolites in blood.