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.

To evaluate the relationship between nonalcoholic fatty liver disease (NAFLD) and coronary artery disease (CAD) and to define determinants of CAD in patients with or without metabolic syndrome. This study was approved by the local ethics committee; informed consent was obtained. Twenty-nine subjects (mean age, 53 years +/- 7 [standard deviation]) with low to intermediate risk for CAD and with fatty liver were included. Thirty-two sex- and age-matched individuals without NAFLD served as controls. CAD was defined as a stenosis of more than 50% in at least one major coronary artery. Fatty liver was assessed by means of an attenuation of -10 HU or higher (calculated as liver attenuation minus spleen attenuation) by using computed tomography (CT), coronary plaques and stenosis by using CT coronary angiography, and biomarkers of insulin resistance, lipotoxicity, systemic inflammation, and oxidant and antioxidant status. A logistic regression analysis was performed to study multivariable associations. When compared with controls, NAFLD patients showed a higher prevalence of calcified and noncalcified coronary plaques (67% vs 34% and 52% vs 29%, respectively; both P < .001), higher prevalence of nonobstructive coronary stenosis (34% vs 14%; P < .008), higher homeostasis model assessment of insulin resistance (3.8 epsilonU/mL +/- 3.6 vs 2.6 epsilonU/mL +/- 3.2; P < .005) and higher triglyceride levels (208 mg/dL +/- 87 vs 148 mg/dL +/- 70; P < .005). Fatty liver proved to be a strong predictor of coronary atherosclerosis (odds ratio [OR], 2; P < .04), independent of indicators for metabolic syndrome (OR, 1.2; P > .2) and C-reactive protein levels (OR, 0.7; P > .4). Patients with NAFLD, even without metabolic syndrome, are at high risk for atherosclerosis. Assessment of NAFLD may be helpful for cardiovascular risk stratification.

Nonalcoholic fatty liver disease (NAFLD) is a common clinical condition which is associated with metabolic syndrome in 70% of cases. Inappropriate dietary fat intake, excessive intake of soft drinks, insulin resistance and increased oxidative stress combine to increase free fatty acid delivery to the liver, and increased hepatic triglyceride accumulation contributes to fatty liver. Regular soft drinks have high fructose corn syrup which contains basic sugar building blocks, fructose 55% and glucose 45%. Soft drinks are the leading source of added sugar worldwide, and have been linked to obesity, diabetes, and metabolic syndrome. The consumption of soft drinks can increase the prevalence of NAFLD independently of metabolic syndrome. During regular soft drinks consumption, fat accumulates in the liver by the primary effect of fructose which increases lipogenesis, and in the case of diet soft drinks, by the additional contribution of aspartame sweetener and caramel colorant which are rich in advanced glycation end products that potentially increase insulin resistance and inflammation. This review emphasizes some hard facts about soft drinks, reviews fructose metabolism, and explains how fructose contributes to the development of obesity, diabetes, metabolic syndrome, and NAFLD.

Olive oil consumption and non-alcoholic fatty liver disease

To examine whether vitamin D improved viral response and predicted treatment outcome in patients with hepatitis C virus (HCV) genotype 2-3. Fifty patients with chronic HCV genotype 2-3 were randomized consecutively into two groups: Treatment group [20 subjects, age 48 ± 14 years, body mass index (BMI) 30 ± 6, 65% male], who received 180 μg pegylated α-interferon-2a plus oral ribavirin 800 mg/d (Peg/RBV), together with oral vitamin D3 (Vitamidyne D drops; 2000 IU/d, 10 drops/d, normal serum level > 32 ng/mL) for 24 wk; and control group (30 subjects, age 45 ± 10 years, BMI 26 ± 3, 60% male), who received identical therapy without vitamin D. HCV RNA was assessed by reverse transcription polymerase chain reaction. Undetectable HCV RNA at 4, 12 and 24 wk after treatment was considered as rapid virological response, complete early virological response, and sustained virological response (SVR), respectively. Biomarkers of inflammation were measured. The treatment group with vitamin D had higher BMI (30 ± 6 vs. 26 ± 3, P < 0.02), and high viral load (> 400,000 IU/mL, 65% vs. 40%, P < 0.01) than controls. Ninety-five percent of treated patients were HCV RNA negative at week 4 and 12. At 24 wk after treatment (SVR), 19/20 (95%) treated patients and 23/30 (77%) controls were HCV RNA negative (P < 0.001). Baseline serum vitamin D levels were lower at baseline (20 ± 8 ng/mL) and increased after 12 wk vitamin D treatment, to a mean level of (34 ± 11 ng/mL). Logistic regression analysis identified vitamin D supplement [odds ratio (OR) 3.0, 95% CI 2.0-4.9, P < 0.001], serum vitamin D levels (< 15 or > 15 ng/mL, OR 2.2, P < 0.01), and BMI (< 30 or > 30, OR 2.6, P < 0.01) as independent predictors of viral response. Adverse events were mild and typical of Peg/RBV. Low vitamin D levels predicts negative treatment outcome, and adding vitamin D to conventional Peg/RBV therapy for patients with HCV genotype 2-3 significantly improves viral response.

Characteristics of common solid liver lesions and recommendations for diagnostic workup