Ethanol concentrations in the human gastrointestinal tract after intake of alcoholic beverages

Abstract

This in vivo study is the first to present intraluminal ethanol concentrations in man after the intake of alcoholic beverages. Relatively low and fast declining gastric ethanol concentrations were observed, contrasting with the current Food and Drug Administration guidelines for the in vitro testing of formulations with respect to ethanol resistance. The presented gastric and duodenal ethanol concentrations and their variation may serve as reference data to design relevant models for predicting (i) ethanol resistance of drug formulations and (ii) ethanol effects on drug solubility and permeability.

Dysregulation of junctional adhesion molecule‐A contributes to ethanol‐induced barrier disruption in intestinal epithelial cell monolayers

“…; Rubbens et al. ). All plates were sealed with parafilm to minimize the loss of ethanol as vapor during the treatment period (Rodriguez et al.…”

“…After overnight incubation at 37°C, monolayers were treated with media, sterile-filtered 200-proof ethanol (6% v/v), or a 1:1 mixed solution of both (3% v/v) to the final volume. These concentrations were based on previously published in vitro and in vivo studies (Ma et al 1999;Tong et al 2013b;Rubbens et al 2016). All plates were sealed with parafilm to minimize the loss of ethanol as vapor during the treatment period (Rodriguez et al 1992).…”

A UFLC–MS/MS method for the simultaneous determination of eight bioactive constituents from red wine and dealcoholized red wine in rat plasma: Application to a comparative pharmacokinetic study

“…It was reported that in volunteers after consumption of alcoholic beverages, ethanol could be monitored in different parts of the gastrointestinal tract. Some 80–90% of alcohol intake arrived at the small intestine, indicating that the whole gastrointestinal tract was affected by alcohol (Rubbens et al, ; Zernig & Battista, ). Qin et al found that acute (chronic) ethanol ingestion might cause intestinal barrier dysfunction by extracting and dissolving lipids from mucus layer, resulting in a decrease in mucosal surface hydrophobicity and an increase in intestinal permeability (Qin & Deitch, ).…”

Variation in gastric alcohol dehydrogenase and the risk of alcohol dependence

“…Badania przeprowadzone na ochotnikach, którzy na czczo spożywali różnego rodzaju napoje alkoholowe, wykazały, że po 90 min od spożycia stężenie alkoholu w świetle żołądka jest mniejsze niż 0,5%, a szybkość opróżniania żołądka w tych warunkach zależy od wielu cech napoju alkoholowego, m.in. spożywanych objętości, wartości pH, kaloryczności, stężenia etanolu oraz właściwości niealkoholowych składników napoju [26]. Czas przebywania alkoholu w żołądku zależy także od innych czynników, takich jak spożycie tłustych pokarmów, intensywny wysiłek fizyczny czy niektóre leki [27].…”

“…the difference between the maximum level of alcohol in the blood estimated with the classic Widmark formula and the actual maximum concentration of alcohol in the blood [10]. Studies conducted in volunteers ingesting various alcoholic beverages under fasting conditions showed that the concentration of alcohol in the gastric lumen 90 minutes after the intake was lower than 0.5%, and the gastric emptying rate in these conditions depended on a variety of alcoholic beverage characteristics such as ingested volumes, pH level, caloric value, ethanol concentration and properties of non-alcoholic ingredients of the consumed beverage [26]. The retention time of alcohol in the stomach also depends on other factors including the consumption of fat-rich foods, intensive physical exercise or certain drugs [27].…”