Effect of Concentration of Ingested Ethanol on Blood Alcohol Levels

Authors

  • Risto P. Roine,

    1. Alcohol Research and Treatment Center and Section of Liver Diseases and Nutrition, Bronx Veterans Affairs Medical Center, and Mount Sinai School of Medicine-CUNY, New York, NY
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  • R. Thomas Gentry,

    1. Alcohol Research and Treatment Center and Section of Liver Diseases and Nutrition, Bronx Veterans Affairs Medical Center, and Mount Sinai School of Medicine-CUNY, New York, NY
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  • Robert T. Lim Jr,

    1. Alcohol Research and Treatment Center and Section of Liver Diseases and Nutrition, Bronx Veterans Affairs Medical Center, and Mount Sinai School of Medicine-CUNY, New York, NY
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  • Enrique Baraona,

    1. Alcohol Research and Treatment Center and Section of Liver Diseases and Nutrition, Bronx Veterans Affairs Medical Center, and Mount Sinai School of Medicine-CUNY, New York, NY
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  • Charles S. Lieber

    Corresponding author
    1. Alcohol Research and Treatment Center and Section of Liver Diseases and Nutrition, Bronx Veterans Affairs Medical Center, and Mount Sinai School of Medicine-CUNY, New York, NY
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  • This study was supported by Department of Health and Human Services Grants AA 03508 and AA 07275 and the Department of Veterans Affairs. Dr. Roine was a recipient of a grant from the Finnish Cultural Foundation.

Reprint requests: Charles S. Lieber, M.D. (ISIG), Alcohol Research and Treatment Center, Veterans Affairs Medical Center, 130 West Kingsbridge Road, Bronx, NY 10468.

Abstract

The effect of the concentration of ingested ethanol on the resulting blood alcohol concentrations (BAC) was tested in both humans and rats. In humans, when 0.3 g/kg body weight ethanol was ingested postprandially, the mean area under the blood alcohol curve (AUC) and the mean peak BAC were significantly lower with a concentrated (40% w/v) than with a dilute (4%) solution. Similarly, rats in the fed state exhibited decreasing mean AUCs with increasing concentrations (4%, 16%, and 40%) of intragastrically administered ethanol (1.0 g/kg). Pharmacokinetic analysis comparing intragastric and intraperitoneal administration of ethanol to rats indicated that the more concentrated solution resulted in less alcohol reaching the systemic circulation (4%: 0.896 ± 0.071 g/kg; 16%: 0.772 ± 0.072 g/kg; 40%: 0.453 ± 0.037 g/kg) and suggested that this effect could be attributed to two factors: increased gastric retention of ethanol (4%: 0.109 ± 0.024 g/kg; 16%: 0.102 2 0.016 g/kg; 40%: 0.214 ± 0.042 g/kg) and a large increase in first-pass metabolism (4%: 0.004 ± 0.054 g/kg; 16%: 0.145 ± 0.048 g/kg; 40%: 0.329 ± 0.044 g/kg).

In contrast to the results in the fed state, in humans fasted overnight the concentration of alcohol consumed (4%, 16%, and 40%) had no significant effect on mean AUCs. In fasted rats, mean AUCs after intragastric intubation of the two lower concentrations of ethanol (4% and 16%) were comparable to those found after intraperitoneal injection, and only the highest ethanol concentration (40%) produced a lower mean AUC.

Our results demonstrate that the consumption of a concentrated solution of ethanol results in lower blood alcohol levels than does a dilute solution, when subjects are tested in the fed state. This effect is associated with more first pass metabolism and less bioavailability with the high ethanol concentrations. These findings now raise the issue whether ethanol in low concentration beverages such as beer and wine has a greater bioavailability than in distilled spirits.

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