Received: 18.06.2012 Accepted: 01.08.2012 J Gastrointestin Liver Dis September 2012 Vol. 21 No 3, 293-302 Address for correspondence: Giovanni Tarantino, MD Dept. Clin. Exp. Medicine Federico II Univ. Medical School Naples, Italy Email: tarantin@unina.it Is there any Consensus as to what Diet or lifestyle Approach Is the Right one for NAFlD Patients? Carmine Finelli 1 , Giovanni Tarantino 1,2 1) Center of Obesity and Eating Disorder, Stella Maris Mediterraneum Foundation, Chiaromonte, Potenza; 2) Department of Clinical and Experimental Medicine, Federico II University Medical School of Naples, Naples, Italy Abstract In this article, we review the current concepts about the pathogenesis of hepatic steatosis and non-alcoholic steatohepatitis and evaluate the existing diets in the context of this knowledge and the available literature. The intent is to enable clinicians to evaluate the diets of non-alcoholic fatty liver disease (NAFLD) patients and make rational decisions based on this perspective - in the absence of controlled trials - to help their patients. Finally, a tailored approach for the dietary treatment of NAFLD is offered as a way to optimize the dietary management of this condition. Key words Non-alcoholic fatty liver disease – non-alcoholic steatohepatitis – diet – hepatic steatosis – type 2 diabetes – insulin resistance. Abbreviations NAFLD: non-alcoholic fatty liver disease; T2D: type 2 diabetes: IR: insulin resistance; HS: hepatic steatosis; NASH: non-alcoholic steatohepatitis; FFA: free fatty acids; TG: triglycerides; DNL: de novo lipogenesis; TNF- α; tumor necrosis factor α; SFA: saturated fatty acids; MUFAs: monounsaturated fatty acids; TC: total cholesterol; PUFAs: polyunsaturated fatty acids; DHA: docosahexaenoic acid; EPA: eicosapentaenoic acid ; PPAR: peroxisome-proliferator activated receptor; SREBP: sterol regulatory element binding protein; GI: glycemic index. REVIEWS Introduction The rising incidence of obesity in today’s environment is associated with many obesity-related health complications, including cardiovascular disease, type 2 diabetes (T2D), hyperlipidemia, hypertension, and non-alcoholic fatty liver disease (NAFLD) [1–4]. This constellation is also recognized as the metabolic syndrome and is characterized by underlying insulin resistance (IR). NAFLD or generally speaking hepatic steatosis (HS) is deined as the accumulation of lipids, primarily in the form of triacylglycerols in individuals who do not consume signiicant amounts of alcohol (<20 g ethanol/day) and in whom other known causes of steatosis, such as certain drugs and toxins, have been excluded [5]. The spectrum of NAFLD includes simple fatty liver, non-alcoholic steatohepatitis (NASH), characterized by inlammation, apoptosis, ballooning degeneration, Mallory hyaline, fibrosis, cirrhosis post NASH, hepatocellular carcinoma and advanced liver disease, which leads to liver- related death [5-10]. Given the close relations between obesity, the metabolic syndrome, and the development of NAFLD, it is not surprising that many NAFLD patients have multiple components of the metabolic syndrome, whether or not they are overweight or obese. Insulin resistance is present in and is a signiicant predictor of NAFLD and NASH in most patients [11], even the ~ 10–15% of patients who are not overweight [12, 13]. NAFLD is a multifactorial disease that involves a complex interaction of genetics, diet, and lifestyle, all of which combine to form the NAFLD phenotype. A cornerstone of the management strategy in such patients with fatty liver is the use of diet to decrease body weight, and improve glycemic control, dyslipidemia and cardiovascular risks as well. There is a bewildering array of diets that have been recommended for the prevention and treatment of all of the components of the metabolic syndrome. Their utility for the treatment of NAFLD remains mostly unknown. It is also important to note that cognitive-behavioral approaches, in addition to dietary modiication, are necessary for the long- term success of dietary and lifestyle interventions.