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Modest alcohol consumption and non-alcoholic steatohepatitis

作者
Rennan Feng,Guoqiang Li,Ying Li,Changhao Sun
出处
期刊:Journal of Hepatology [Elsevier BV]
卷期号:57 (6): 1392-1393
标识
DOI:10.1016/j.jhep.2012.06.040
摘要

Modest alcohol consumption is associated with decreased prevalence of steatohepatitis in patients with non-alcoholic fatty liver disease (NAFLD)Journal of HepatologyVol. 57Issue 2PreviewNon-alcoholic fatty liver disease (NAFLD) is a cardiovascular risk factor. Although modest alcohol consumption may reduce the risk for cardiovascular mortality, whether patients with NAFLD should be allowed modest alcohol consumption remains an important unaddressed issue. We aimed to evaluate the association between modest alcohol drinking and non-alcoholic steatohepatitis (NASH), among subjects with NAFLD. Full-Text PDF Reply to: “Modest alcohol consumption and non-alcoholic steatohepatitis”: Measure, modesty, and mechanism: Alcohol in non-alcoholic steatohepatitisJournal of HepatologyVol. 57Issue 6PreviewWe studied the association of modest alcohol consumption and steatohepatitis in a large sample of well-characterized study participants with biopsy-proven non-alcoholic fatty liver disease (NAFLD) from referral centers across the United States. Modest alcohol consumption was associated with significantly lower odds of non-alcoholic steatohepatitis (NASH). Feng et al. raise questions about diabetes and soft drink consumption as potential confounders. Full-Text PDF Open Access We read with great interest the article by Dunn et al., published in March 2012 [[1]Dunn W. Sanyal A.J. Brunt E.M. Unalp-Arida A. Donohue M. McCullough A.J. et al.Modest alcohol consumption is associated with decreased prevalence of steatohepatitis in patients with non-alcoholic fatty liver disease (NAFLD).J Hepatol. 2012; 57: 384-391Abstract Full Text Full Text PDF PubMed Scopus (209) Google Scholar]. This cross-sectional study reported some interesting observations on the relationship between modest alcohol consumption and non-alcoholic steatohepatitis (NASH). However, the study has some limitations. Dunn et al., clearly demonstrated that modest alcohol consumption was significantly inversely associated with NASH, which was consistent with other recent studies [2Hamaguchi M. Kojima T. Ohbora A. Takeda N. Fukui M. Kato T. Protective effect of alcohol consumption for fatty liver but not metabolic syndrome.World J Gastroenterol. 2012; 18: 156-167Crossref PubMed Scopus (74) Google Scholar, 3Moriya A. Iwasaki Y. Ohguchi S. Kayashima E. Mitsumune T. Taniguchi H. Ikeda F. Yamamoto K. Impact of alcohol consumption on the presence, development of fatty liver in men and women.J Hepatol. 2011; 54: S209-S361Abstract Full Text PDF PubMed Google Scholar]. However, some important confounding factors were not considered or discussed. First, the rate of diabetes in the lifetime non-drinkers was significantly higher than that of modest drinkers (37.5% vs. 22.1%), but this was not included as a covariant in the multiple logistic regression analysis. As subjects with diabetes are more prone to have fatty liver disease, this difference should be considered in the analysis. Second, soft drinks consumption might also be an important factor. Early studies have reported that soft drinks, especially fructose, contribute to the development of diabetes and non-alcoholic fatty liver disease (NAFLD) [[4]Nseir W. Nassar F. Assy N. Soft drinks consumption and nonalcoholic fatty liver disease.World J Gastroenterol. 2010; 16: 2579-2588Crossref PubMed Scopus (148) Google Scholar]. In addition, lifetime non-drinkers may drink more soft drinks than modest drinkers do, which may also affect the result. However, this confounding factor was not mentioned or discussed in the article either. Third, as the mechanisms of the inverse association between alcohol consumption and NAFLD or NASH are still unclear, genetic factors might be the answer to this question. Alcohol consumption might interact with some genetic factors and lead to NAFLD or NASH. We believe the authors have considered this and investigated several SNPs, finding that PNPLA3 genotype was significantly different between the two groups. Again, this polymorphism was not included in the multiple logistic regression analysis. Thus, in our opinion, future studies should consider all the above mentioned factors, which would help interpret their important findings. The authors declared that they do not have anything to disclose regarding funding or conflict of interest with respect to this manuscript. Supported by the National High Technology Research and Development Program of China (863 program) (No. 2010AA023002) and the National Natural Science Foundation of China (No. 81202184).

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