Obesity and female gender increase breath ethanol concentration: Potentialimplications for the pathogenesis of nonalcoholic steatohepatitis

OBJECTIVES: Similarities between histological features of alcoholic hepatit is and obesity-related liver disease suggest a common pathogenic mechanism. Because intestinal bacteria can produce ethanol, it is conceivable that in testinally derived alcohol may contribute to fatty liver disease. An indire ct way of measuring endogenous ethanol is to measure the breath ethanol con centration. In a previous study in ob/ob mice, breath ethanol decreased wit h a course of nonabsorbable antibiotics, suggesting that the ethanol is der ived from intestinal bacterial flora. The aims of this study were 1) to det ermine whether alcohol can be detected in the breath of human subjects, and 2) to assess whether there is any correlation between ethanol and obesity in patients with nonalcoholic steatohepatits (NASH) and control subjects wi thout known liver disease. METHODS: Breath ethanol concentration was determined in 21 patients with bi opsy-proven NASH and in 10 control subjects by gas chromatography. An abnor mal breath ethanol level was defined as two standard deviations above the m ean value of the breath ethanol of lean controls. RESULTS: Minute quantities of ethanol were detected in the breath of human subjects who had not consumed alcohol in the recent past. Patients who were obese were more likely to have higher breath ethanol concentrations. Women also had higher breath alcohol than men. However, there was no difference between patients with NASH and controls. Severity of liver disease, as evid enced by cirrhosis, did not influence the breath ethanol concentration. CONCLUSIONS: Higher breath ethanol concentrations are observed in obese sub jects than in leaner ones. It is possible that intestinally derived ethanol may contribute to the pathogenesis of NASH. (Am J Gastroenterol 2001;96:12 00-1204. (C) 2001 by Am. Coll. of Gastroenterology).