In order to assess the inter-relationship between nutritional intake and alcohol consumption on the risk of liver cirrhosis we performed a hospital-based retrospective case-control study. We enrolled 115 cases admitted to hospital for liver decompensation at their first diagnosis of liver cirrhosis and 167 hospital controls without evidence of liver disease admitted for acute diseases unrelated to alcohol intake. Daily alcohol intake and average nutrient intake were measured throughout the patient's life, using a reproducible questionnaire. No dose-effect relationship was found between nutrient intake and risk of cirrhosis using classical association statistical methods. We then corrected the intake of each nutrient for the total caloric intake and this energy-adjusted nutrient intake was used in a logistic regression model together with alcohol intake, viral B and C hepatitis markers, age and gender. Using this approach, carbohydrates intake were shown to have a protective effect on the risk of cirrhosis, whereas saturated lipid intake had a significant multiplicative effect on the risk associated with alcohol consumption. By comparison with the teetotalers category who had an average daily intake of saturated fatty acids lower than 40.3 g (reference category; OR = 1), drinkers of more than 100 g ethanol per day showed ORs ranging from 14.2 (95% confidence interval 2.0-101.0) for consumers of less than 40.3 g fatty acid per day, to 39.0 (95% confidence interval 5.0-305.1) for consumers of more than 40.4 g fatty acid per day. In conclusion we give additional evidence on the relationship between diet and risk of cirrhosis, whereby saturated lipid intake multiplies the risk associated with alcohol intake. However, caution should be used to interpret such results, since they seem to suggest that diet but not a particular nutrient can modify the effect of alcohol on the risk of cirrhosis. The present lack of agreement on the mechanisms and the nutrients involved in the pathogenesis of alcoholic liver injury should stimulate wider epidemiological studies using modern nutritional techniques.
Corrao, G., Lepore, A., Torchio, P., Galatola, G., Aricò, S., Di Orio, F. (1995). Interaction between dietary pattern and alcohol intake on the risk of liver cirrhosis. The Provincial Group for the Study of Chronic Liver Disease. REVUE D'EPIDEMIOLOGIE ET DE SANTE PUBLIQUE, 43(1), 7-17.
Interaction between dietary pattern and alcohol intake on the risk of liver cirrhosis. The Provincial Group for the Study of Chronic Liver Disease
CORRAO, GIOVANNI;
1995
Abstract
In order to assess the inter-relationship between nutritional intake and alcohol consumption on the risk of liver cirrhosis we performed a hospital-based retrospective case-control study. We enrolled 115 cases admitted to hospital for liver decompensation at their first diagnosis of liver cirrhosis and 167 hospital controls without evidence of liver disease admitted for acute diseases unrelated to alcohol intake. Daily alcohol intake and average nutrient intake were measured throughout the patient's life, using a reproducible questionnaire. No dose-effect relationship was found between nutrient intake and risk of cirrhosis using classical association statistical methods. We then corrected the intake of each nutrient for the total caloric intake and this energy-adjusted nutrient intake was used in a logistic regression model together with alcohol intake, viral B and C hepatitis markers, age and gender. Using this approach, carbohydrates intake were shown to have a protective effect on the risk of cirrhosis, whereas saturated lipid intake had a significant multiplicative effect on the risk associated with alcohol consumption. By comparison with the teetotalers category who had an average daily intake of saturated fatty acids lower than 40.3 g (reference category; OR = 1), drinkers of more than 100 g ethanol per day showed ORs ranging from 14.2 (95% confidence interval 2.0-101.0) for consumers of less than 40.3 g fatty acid per day, to 39.0 (95% confidence interval 5.0-305.1) for consumers of more than 40.4 g fatty acid per day. In conclusion we give additional evidence on the relationship between diet and risk of cirrhosis, whereby saturated lipid intake multiplies the risk associated with alcohol intake. However, caution should be used to interpret such results, since they seem to suggest that diet but not a particular nutrient can modify the effect of alcohol on the risk of cirrhosis. The present lack of agreement on the mechanisms and the nutrients involved in the pathogenesis of alcoholic liver injury should stimulate wider epidemiological studies using modern nutritional techniques.
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