The effect of alcohol consumption on the liver is controversial. Recent reports have suggested that moderate alcohol consumption decreases the prevalence of elevated alanine aminotransferase levels. The role of alcohol consumption in the development of fatty liver (FL), however, has not been studied definitively. The aim of this study was to examine the association between alcohol consumption and FL in a large Japanese population.
A total of 7,431 asymptomatic male subjects who underwent a complete medical survey in our institute between May 2007 and July 2008 were recruited. Cases positive for hepatitis B or C viruses, potential hepatotoxic drug intake, or under treatment for metabolic disorders were excluded. FL was defined by ultrasonography. Visceral and subcutaneous adipose tissues (VAT and SAT) were measured by computed tomography. Independent and significant predictors associated with FL were determined by multiple logistic regression analysis.
Of the initial study candidates, 130 (1.7%) were positive for hepatitis B and 66 (0.8%) were positive for hepatitis C. On the basis of the inclusion and exclusion criteria, 5,599 men (50.9+/-8.1 years) were studied cross-sectionally. Light (40-140 g/week) and moderate (140-280 g/week) alcohol consumption significantly and independently reduced the likelihood of FL (odds ratio=0.824 and 0.754, 95% confidence interval=0.683-0.994 and 0.612-0.928, P=0.044 and 0.008, respectively) by multivariate analysis after adjusting for potential confounding variables. VAT, SAT, low-density lipoprotein, triglycerides, and fasting blood glucose were significant predictors of the increased prevalence of FL, whereas age was a predictor of the decreased prevalence of FL.
The prevalence of FL was significantly and independently decreased by light and moderate alcohol consumption in men of an asymptomatic Japanese population.
"Clinical studies have suggested that light or moderate (<10–20 g ethanol/day) alcohol intake protects against NAFLD . Light alcohol consumption (20 g ethanol on 1–3 days/week or 40–140 g ethanol/week) and moderate alcohol consumption (140–280 g ethanol/week) were independently associated with a low prevalence of fatty liver [155, 156], whereas moderate to heavy drinking (>60 g ethanol/week) was associated with the progression of hepatic steatosis and fibrosis [157, 158]. "
[Show abstract][Hide abstract] ABSTRACT: Nonalcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) are multidisciplinary liver diseases that often accompany type 2 diabetes or metabolic syndrome, which are characterized by insulin resistance. Therefore, effective treatment of type 2 diabetes and metabolic syndrome should target not only the cardiometabolic abnormalities, but also the associated liver disorders. In the last decade, it has been shown that metformin, thiazolidinediones, vitamin E, ezetimibe, n-3 polyunsaturated fatty acids, renin-angiotensin system (RAS) blockers, and antiobesity drugs may improve hepatic pathophysiological disorders as well as clinical parameters. Accordingly, insulin sensitizers, antioxidative agents, Niemann-Pick C1-like 1 (NPC1L1) inhibitors, RAS blockers, and drugs that target the central nervous system may represent candidate pharmacotherapies for NAFLD and possibly NASH. However, the efficacy, safety, and tolerability of long-term treatment (potentially for many years) with these drugs have not been fully established. Furthermore, clinical trials have not comprehensively examined the efficacy of lipid-lowering drugs (i.e., statins, fibrates, and NPC1L1 inhibitors) for the treatment of NAFLD. Although clinical evidence for RAS blockers and incretin-based agents (GLP-1 analogs and dipeptidyl peptidase-4 inhibitors) is also lacking, these agents are promising in terms of their insulin-sensitizing and anti-inflammatory effects without causing weight gain.
"There is no evidence that alcohol abstinence is beneficial for patients with NAFLD/NASH. In fact studies have shown an inverse association between modest wine drinking (less than a glass a day) and biochemical  , ultrasonographic  or histologic  evidence of NAFLD/NASH with protective effects on diabetes, IR, and features of the metabolic syndrome   . "
[Show abstract][Hide abstract] ABSTRACT: Histological analysis of liver biopsies remains a standard against which other methods of assessment for the presence and amount of hepatic injury due to nonalcoholic fatty liver disease (NAFLD) are measured. Histological evaluation remains the sole method of distinguishing steatosis from advanced forms of NAFLD, i.e. nonalcoholic steatohepatitis (NASH) and fibrosis. Included in the lesions of NAFLD are steatosis, lobular and portal inflammation, hepatocyte injury in the forms of ballooning and apoptosis, and fibrosis. However, patterns of these lesions are as distinguishing as the lesions themselves. Liver injury in adults and children due to NAFLD may have different histological patterns. In this review, the rationale for liver biopsy, as well as the histopathological lesions, the microscopically observable patterns of injury, and the differential diagnoses of NAFLD and NASH are discussed.
World Journal of Gastroenterology 01/2010; 16(42). DOI:10.3748/wjg.v16.i42.5286 · 2.37 Impact Factor
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