Alcohol Consumption and Alcoholic Liver Disease: Evidence of a Threshold Level of Effects of Ethanol
Article first published online: 29 JUN 2007
Alcoholism: Clinical and Experimental Research
Volume 17, Issue 5, pages 1112–1117, September 1993
How to Cite
Savolainen, V. T., Liesto, K., Männikkö, A., Penttilä, A. and Karhunen, P. J. (1993), Alcohol Consumption and Alcoholic Liver Disease: Evidence of a Threshold Level of Effects of Ethanol. Alcoholism: Clinical and Experimental Research, 17: 1112–1117. doi: 10.1111/j.1530-0277.1993.tb05673.x
- Issue published online: 29 JUN 2007
- Article first published online: 29 JUN 2007
- Received for publication January 20, 1993; accepted April 16, 1993
- Alcohol Consumption;
- Liver Cirrhosis;
- Alcoholic Liver Disease;
The effects of long-term moderate or “social” alcohol consumption (10-80 g daily intake) on the incidence of features of alcoholic liver disease (ALD) were delineated in a consecutive autopsy series of 210 males. The subjects' daily intake, as well as duration of alcohol consumption, was determined by an interview with the spouse or a close acquaintance and compared with semiquantitative histological scores for stage of ALD.
No significant increase in the incidence of features of ALD could be related to all-year daily intake of ethanol below 40 g (40 g equals 1.1 liter of beer, 0.44 liter of wine, and 0.11 liter of spirits). However, daily intake between 40–80 g increased relative liver weight on average 3.1 g/kg of body weight (p < 0.02), the frequency of fatty liver from 11.7 to 47.2% [relative risk (RR) = 4.4], and the frequency of mainly slight alcoholic hepatitis up to 16.7% (RR = 7.5). The incidence of both bridging fibrosis and liver cirrhosis increased significantly (RR = 8.8) only when daily intake exceeded 80 g. Amounts of ethanol exceeding 80 g did not relate to further increases in incidence of bridging fibrosis or liver cirrhosis.
These findings suggest that, in males, daily ingestion of ethanol below 40 g for a period of 25 years does not increase the risk of alcohol-related liver disease. In contrast, similar duration of daily intake between 40 and 80 g (mean 61.6 g) increased the risk of all but fibrotic liver lesions of ALD significantly and may thus represent a potential threshold level that significantly increases the risk of alcohol-related liver damage. Moreover, our results may suggest that, on an individual level, the risk function for liver fibrosis may not be directly dose-related, but rather, when a permissive threshold level is attained, further consumption is of no or little importance to the progression of ALD.