Dietary habits and nutrient intake in non-alcoholic steatohepatitis

Toshimitsu, Kumiko; Matsuura, Bunzo; Ohkubo, Ikuko; Niiya, Tetsuji; Furukawa, Shinya; Hiasa, Yoichi; Kawamura, M.; Ebihara, Kiyoshi; Onji, Morikazu

doi:10.1016/j.nut.2006.09.004

Cited by 230 publications

(199 citation statements)

References 36 publications

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“…18,19 Several studies have highlighted the fact that dietary intake rich in saturated fat and cholesterol and sweet carbohydrates was associated with NAFLD. 20,21 Fast food and soft drinks contain artificial sweeteners, such as fructose. Results of several recent studies suggest that an increased intake of dietary fructose may be associated with the development of NAFLD.…”

Section: Singh Et Al Risk Factors Associated With Non-alcoholic Fattymentioning

confidence: 99%

Risk Factors Associated With Non-Alcoholic Fatty Liver Disease in Indians: A Case–Control Study

Singh

Misra

et al. 2015

Journal of Clinical and Experimental Hepatology

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Background/Aims: NAFLD has today emerged as the leading cause of liver disorder. There is scanty data on risk factors associated with NAFLD emanating from India. The present study was conducted to identify the risk factors associated with NAFLD. Methods: 464 consecutive NAFLD patients and 181 control patients were subjected to detailed questionnaire regarding their lifestyle and dietary risk factors. Anthropometric measurements were obtained and biochemical assays were done. Comparison of different variables was made between NAFLD patients and controls using principal component analysis (PCA). Results: NAFLD patients had higher BMI [26.25 AE 3.80 vs 21.46 AE 3.08 kg/m 2 , P = 0.000], waist-hip ratio [0.96 AE 0.12 vs 0.90 AE 0.08, P = 0.000] and waist-height ratio [0.57 AE 0.09 vs 0.50 AE 0.06, P = 0.000] compared to controls. Fasting blood sugar [101.88 AE 31.57 vs 90.87 AE 10.74 mg/dl] and triglyceride levels [196.16 AE 102.66 vs 133.20 AE 58.37 mg/dl] were significantly higher in NAFLD group. HOMA-IR was also higher in NAFLD group [2.53 AE 2.57 vs 1.16 AE 0.58, P = 0.000]. Majority (90.2%) of NAFLD patients were sedentary. Family history of metabolic syndrome (MS) was positively correlated with NAFLD. Dietary risk factors associated with NAFLD were non-vegetarian diet [35% vs 23%, P = 0.002], fried food [35% vs 9%, P = 0.000], spicy foods [51% vs 15%, P = 0.001] and tea [55% vs 39%, P = 0.001]. Diabetes, hypertension, snoring and sleep apnoea syndrome were common factors in NAFLD. On multivariate PCA, waist/height ratio and BMI were significantly higher in the NAFLD patients. Conclusion: The risk factors associated with NAFLD are sedentary lifestyle, obesity family history of MS, consumption of meat/fish, spicy foods, fried foods and tea. Other risk factors associated with NAFLD included snoring and MS. ( J CLIN EXP HEPATOL 2015;5:295-302) N on-alcoholic fatty liver disease (NAFLD) is a distinct clinico-pathologic entity characterized histologically by a spectrum ranging from simple steatosis to steatohepatitis (NASH), cirrhosis and even hepatocellular carcinoma (HCC). 1,2 NAFLD (steatosis of the liver) is highly prevalent in Western countries. 1 With the introduction of westernized lifestyle and the increasing frequency of obesity in the Asia-Pacific region, the prevalence of NAFLD has increased over the past two decades.Studies from different regions of India have shown that NAFLD is very common in Indians. [3][4][5] Risk factors implicated in the development of NAFLD are obesity and metabolic syndrome (MS). 6,7 However, it is obvious that NAFLD is multifactorial and identifying the various risk factors associated with NAFLD in our population could help us to intervene in order to prevent its progression to more severe forms of the disease.The few studies identifying the risk factors associated with NAFLD have emanated from the West, where the profiles of NAFLD patients appear to be different. [8][9][10] The observed differences in Indian NAFLD patients include a lower frequency of MS, 9,11 lesser degree ...

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Section: Singh Et Al Risk Factors Associated With Non-alcoholic Fattymentioning

confidence: 99%

Risk Factors Associated With Non-Alcoholic Fatty Liver Disease in Indians: A Case–Control Study

Singh

Misra

et al. 2015

Journal of Clinical and Experimental Hepatology

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“…Indeed, results of several human studies suggest that a high intake of carbohydrates is associated with the development of NAFLD and may increase the odds of developing later, more severe stages of the disease (e.g., nonalcoholic steatohepatitis [NASH]). 4,5 Furthermore, it has recently been shown that in patients with NAFLD (e.g., with simple steatosis and steatohepatitis with begin-ning fibrosis) intake of fructose is markedly higher than in controls. 6,7 In line with these findings it has been shown in animal studies that an increased consumption of fructose (e.g., up to 60% of daily calories derived from fructose) may result in hepatic steatosis accompanied by insulin resistance, elevated plasma triglyceride levels, and oxidative stress in the liver.…”

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confidence: 99%

Toll-like receptor 4 is involved in the development of fructose-induced hepatic steatosis in mice

et al. 2009

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A link between dietary fructose intake, gut-derived endotoxemia, and nonalcoholic fatty liver disease (NAFLD) has been suggested by the results of human and animal studies. To further investigate the role of gut-derived endotoxin in the onset of fructose-induced NAFLD, Toll-like receptor (TLR-) 4-mutant (C3H/HeJ) mice and wildtype (C3H/HouJ) mice were either fed plain water or water enriched with 30% fructose for 8 weeks. Hepatic steatosis, plasma alanine aminotransferase (ALT), and markers of insulin resistance as well as portal endotoxin levels were determined. Hepatic levels of myeloid differentiation factor 88 (MyD88), interferon regulatory factor (IRF) 3 and 7, and tumor necrosis factor alpha (TNF␣) as well as markers of lipid peroxidation were assessed. Chronic intake of 30% fructose solution caused a significant increase in hepatic steatosis and plasma ALT levels in wildtype animals in comparison to water controls. In fructose-fed TLR-4 mutant mice, hepatic triglyceride accumulation was significantly reduced by Ϸ40% in comparison to fructose-fed wildtype mice and plasma ALT levels were at the level of water-fed controls. No difference in portal endotoxin concentration between fructose-fed wildtype and TLR-4-mutant animals was detected. In contrast, hepatic lipid peroxidation, MyD88, and TNF␣ levels were significantly decreased in fructose-fed TLR-4-mutant mice in comparison to fructose-fed wildtype mice, whereas IRF3 and IRF7 expression remained unchanged. Markers of insulin resistance (e.g., plasma TNF␣, retinol binding protein 4, and hepatic phospho-AKT) were only altered in fructose-fed wildtype animals. Conclusion: Taken together, these data further support the hypothesis that in mice the onset of fructose-induced NAFLD is associated with intestinal bacterial overgrowth and increased intestinal permeability, subsequently leading to an endotoxin-dependent activation of hepatic Kupffer cells.

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“…However, there are few published reports on the intake of various nutrients in patients with NAFLD. Recently, it has been reported that patients with fatty liver consume more simple carbohydrates and less saturated fat than those in the general population, suggesting that imbalanced diets play important roles in the development and progression of NAFLD, and that correction of these diets may be necessary (7).…”

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confidence: 99%

Soft Drink Consumption Linked with Fatty Liver in the Absence of Traditional Risk Factors

Assy

Nasser

Kamayse

et al. 2008

Canadian Journal of Gastroenterology

290

194

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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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Dietary habits and nutrient intake in non-alcoholic steatohepatitis

Cited by 230 publications

References 36 publications

Risk Factors Associated With Non-Alcoholic Fatty Liver Disease in Indians: A Case–Control Study

Risk Factors Associated With Non-Alcoholic Fatty Liver Disease in Indians: A Case–Control Study

Toll-like receptor 4 is involved in the development of fructose-induced hepatic steatosis in mice

Soft Drink Consumption Linked with Fatty Liver in the Absence of Traditional Risk Factors

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