The differing effects of acute and chronic alcohol on gastric and intestinal permeability

Acute and chronic alcohol intake cause GI symptoms because of either alcohol-induced structural or functional abnormalities. In theory, the disruption of the integrity of the gut mucosa should be reflected by changes in the absorption of molecular probes, such as lactulose, mannitol, and sucrose. Accordingly, we investigated the effects of acute and chronic ethanol on the permeability of the gastric and small intestinal mucosa.

We measured the absorption of sucrose, mannitol, and lactulose in 20 controls and 18 alcoholics within 3 days after their last drink. We evaluated the reversibility of the abnormalities in alcoholics by repeat testing after 7 to 14 days of sobriety. The acute effects of ethanol in normal controls and abstinent alcoholics were also studied after the administration of ethanol by both the oral and IV routes.

The absorptions of lactulose and sucrose in chronic alcoholics were normal. However, the alcoholics demonstrated a significant decrease in mannitol absorption and a corresponding increase in the lactulose/mannitol ratio. Both parameters returned to normal after a period of sobriety. Acute ethanol did not significantly affect mannitol or lactulose absorption, whereas oral ethanol significantly increased sucrose absorption.

Chronic ethanol reversibly affects the integrity of small intestinal villi without significantly affecting gastrointestinal permeability. In contrast, a single oral dose of ethanol increases gastroduodenal permeability but has no effect on the lactulose or mannitol permeability of the small intestine. These regional changes in gut permeabilities may contribute to alcohol-induced GI symptoms.