Assy, N. et al. Soft drink consumption linked with fatty liver in the absence of traditional risk factors. Can. J. Gastroenterol. 22, 811-816

Liver Unit, Ziv Medical Center, Safed, Israel.
Canadian journal of gastroenterology = Journal canadien de gastroenterologie (Impact Factor: 1.98). 11/2008; 22(10).
Source: PubMed Central


Background: Little is known about dietary habits and their relationships with liver disease in nonalcoholic fatty liver disease (NAFLD) patients, particularly in the absence of obesity, diabetes or hyperlipidemia. Objective: To assess the association between soft drink consumption and the presence of fatty liver in NAFLD patients who do not have classic risk factors. Methods: Three hundred ten patients with NAFLD diagnosed by ultrasound were assessed for 36 months in a cross-sectional manner. Thirty-one patients (10%) who had NAFLD without classic risk factors were compared with 30 healthy controls. Physical activity was assessed during the preceding week and year, and every six months for 36 months. Data on daily dietary intake of food and soft drink, and the source of added sugar were collected during two seven-day periods, at the beginning of the study, and within two weeks after the metabolic tests by using a validated food questionnaire given by a trained dietician. Insulin resistance and lipid peroxidation were assessed by homeostasis model assessment-insulin resistance index (HOMA-IRI) and malondialdehyde (MDA) levels, respectively. Results: Eighty per cent of patients (25 of 31) consumed an excessive amount of soft drink beverages (more than 50 g/day of added sugar) for 36 months, compared with 20% in healthy controls (P<0.001). Twenty per cent of patients consumed one drink per day, 40% consumed two to three drinks per day, and 40% consumed more than four drinks per day for most days during 36 months. The most common soft drinks consumed were regular Coca-Cola (40% of patients), Diet Coke (40%) and flavoured fruit juices (20%). Ultrasound findings revealed mild fatty liver in 44% of cases (n=14), moderate fatty liver in 38% (n=12), and severe fatty liver in 18% (n=5). HOMA-IRI and MDA levels were significantly higher in patients with NAFLD than in healthy controls (HOMA-IRI, 3.7 versus 1.7, P<0.001; and MDA, 420±300 μmol/mL versus 200±100 μmol/mL; P<0.001). When controlled for other factors, including dietary composition and physical activity, soft drink beverage consumption was the only independent variable that was able to predict the presence of fatty liver in 82.5% of cases with a sensitivity of 100%, a specificity of 76%, a positive predictive value of 57% and a negative predictive value of 100%. Conclusion: The present study may add important insight into the role of sugar-sweetened beverage consumption as a cause of fatty liver in patients without risk factors. Patients are encouraged to change their long-standing drinking behaviour.

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    • "Accordingly, caloric restriction (combined or not with increased physical activity) or hypocaloric diets were shown to be efficient in reducing hepatic steatosis in both type 2 diabetic subjects and NAFLD patients (Elias et al., 2010; Haufe et al., 2011; Lazo et al., 2010). Finally, it has been shown in 31 NAFLD-diagnosed subjects without classic risk factors that soft drink beverage consumption was the only independent variable predicting fatty liver in 82.5% of subjects (Assy et al., 2008). It is also worth mentioning that copper deficiency may predispose individuals to hepatic steatosis, as shown in 140 NAFLD patients (Aigner et al., 2008). "
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    ABSTRACT: Hepatic steatosis is a lipid metabolic deregulation that affects millions of people worldwide and that may lead to more severe chronic liver diseases such as steatohepatitis, hepatic fibrosis, cirrhosis, or cancer. Surprisingly, the potential of diets, food groups, foods, and/or compounds to prevent hepatic steatosis prevalence has been only rarely studied in humans. The reasons for this are unclear. Yet, plant- and animal-based foods contain several bioactive compounds that are able to limit excess fat deposits, mainly triglycerides; they are called lipotropes and are used in commercial nutritional complements such as fat burners or lipotropic complexes. Although the most recognized lipotropes are choline, betaine, myo-inositol, and methionine, and to a lesser extent carnitine, many other food compounds have the ability to exert a lipotropic effect, e.g. some B vitamins, polyphenols, fiber, and organosulfur compounds. However, while most studies have been carried out in animal models of steatosis, the few human studies that have been conducted were concerned mainly with beverages like coffee or tea and with isolated lipotropes like betaine, carnitine, and polyunsaturated fatty acids. Studies associating solid food groups or dietary patterns with hepatic steatosis have almost never been performed. Therefore, the main objectives of this chapter will be to examine the state-of-the art about human studies and lipotrope consumption, and to discuss the lipotropic potential of food products with emphasis on grain products that are both cheap and lipotrope-dense foods. The adequacy between real lipotrope consumption and human needs will also be discussed.
    Full-text · Chapter · Sep 2014
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    • "NAFLD is defi ned as the accumulation of lipid, primarily triacylglycerols, in the liver [McCullough, 2004]. Soft drink consumption was associated with NAFLD independent of metabolic syndrome [Abid et al., 2009] or in the absence of traditional risk factors, including obesity, diabetes or hyperlipidemia [Assy et al., 2008]. "
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    ABSTRACT: Nonalcoholic steatohepatitis (NASH) and nonalcoholic fatty liver disease are increasing in adults and are likely to be increasing in children. The aim of the present research was to evaluate the protective effect of rice bran oil and pumpkin seed oil against high fructose diet (HFD) inducing nonalcoholic steatohepatitis (NASH). The results showed signifi cant elevation of plasma total and direct bilirubin, transaminases activities, total cholesterol (T-Ch), triglycerides (TG), low density lipoprotein-cholesterol (LDL-Ch), tumor necrosis factor- (TNF-) and malondialdehyde (MDA) with signifi cant increase in liver TG, T-Ch and MDA along with signifi cant reduction in plasma high density lipoprotein cholesterol (HDL-Ch) and increase in T-Ch/HDL-Ch in rats fed HFD compared to rats fed on balanced diet. Histopathology of liver of rats fed on HFD confi rmed the induction of NASH. Rice bran oil and pumpkin seed oil produced improvement in the biochemical parameters with different degrees. Pumpkin seed oil reversed all histopathological changes that occur in liver tissue which became comparable to normal in some rats. In conclusion, rats fed high fructose diet are a good model for studying NASH. Rice bran oil and pumpkin seed oil afford hepato protection against NASH in rat model.
    Full-text · Article · Jun 2014 · Polish Journal of Food and Nutrition Sciences
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    • "The increased consumption of fructose temporally parallels the increased prevalence of obesity and the metabolic syndrome in the United States and worldwide (4, 5). Emerging evidence has shown that high fructose intake may play an important role in the development of NAFLD (6, 7). "
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    ABSTRACT: Objective Dietary fructose and copper interaction may play an important role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). In this study, we investigate whether or not modest fructose consumption (3% fructose, w/v) (which is more closely related to the American lifestyle with regard to sugar beverage consumption) affects copper status, and causes liver injury and fat accumulation in marginal copper deficient rats. Design and Methods Male weanling Sprague-Dawley rats were fed either an adequate copper (6ppm) or a marginally copper deficient (1.6ppm) diet for 4 weeks. Deionized water or deionized water containing 3% fructose (w/v) was given ad lib. Results Modest fructose consumption further impaired copper status in the marginal copper deficient rats and increased hepatic iron accumulation. Liver injury and fat accumulation were significantly induced in the marginal copper deficient rats exposed to fructose. Conclusions Our data suggest that modest fructose consumption can impair copper status and lead to hepatic iron overload, which in turn, may lead to liver injury and fatty liver in marginal copper deficient rats. This study provides important information on dietary fructose and copper interaction, suggesting that dietary fructose induced low copper availability might be an important mechanism underlying fructose induced fatty liver.
    Full-text · Article · Aug 2013 · Obesity
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