Alterations in ethyl alcohol pharmacokinetics during oral consumption of malt liquor beverages in African Americans

Background: Malt liquor (ML) beverages have become increasingly popular among urban minority groups, due partly to their inexpensive price and targeted advertising. We hypothesized that nonfermented by‐products contained in ML beverages will alter the pharmacokinetics (PK) and pharmacodynamic (PD) effects of its ethanol content. In addition, we determined the effect of alcohol dehydrogenase (ADH) genotypes on the PK following consumption of ML beverages. Methods: The study was conducted in 31 healthy adult African‐American social drinkers, mean ± SD age of 22.3 ± 1.3 years, and weight of 70.7 ± 10.9 kg. Participants were administered ethanol, in randomized order, 2‐weeks apart, in the form of oral ML beverage (6%v/v), or isocaloric solution of diet soda–ethanol (DS–Etoh) beverage (6%v/v). During each session the beverage was consumed over 4 minutes and breath alcohol concentrations (BrAC) as well as subjective and behavioral effects of ethanol were evaluated over 180 minutes. Pharmacokinetic parameters of ethanol were calculated using Michaelis–Menten elimination kinetics. The effect of ML and ADH genotype on PK was evaluated using the Wilcoxon rank‐sum test and the Wilcoxon signed rank test, respectively. Results: Results show a slower mean rate of absorption, K_a, (0.12 vs. 0.15 min^?1, p = 0.03) and a longer time to reach maximum concentration, T_max, (28 vs. 23 minute, p < 0.01) for the ML compared with DS–Etoh beverage. The ML beverage resulted in a larger area under the BrAC–time curve compared with DS–Etoh beverage (8.4 vs. 6.8 min g/dl, p = 0.02). There was no difference in the subjective PD effects between the 2 beverages. Conclusion: Results show that exposure to ethanol following the consumption of ML beverages is different compared to that following nonmalt beverages in African‐Americans. These differences may be related to nonfermented by‐products present in commercially available ML products. These PK differences do not appear to result in significant perceived alcohol PD changes, nor are they related to ADH genotype.