Diet, weight loss, and liver health in nonalcoholic fatty liver disease: Pathophysiology, evidence, and practice

  title={Diet, weight loss, and liver health in nonalcoholic fatty liver disease: Pathophysiology, evidence, and practice},
  author={Giulio Marchesini and Salvatore Petta and Riccardo Dalle Grave},
Fatty liver accumulation results from an imbalance between lipid deposition and removal, driven by the hepatic synthesis of triglycerides and de novo lipogenesis. The habitual diet plays a relevant role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD), and both risky (e.g., fructose) and protective foods (Mediterranean diet) have been described, but the contribution of excess calories remains pivotal. Accordingly, weight loss is the most effective way to promote liver fat removal… 

Nutritional Approaches to Achieve Weight Loss in Nonalcoholic Fatty Liver Disease.

Weight loss is crucial to the improvement of NAFLD and NASH, and patients should attempt various diets in an attempt to achieve weight loss.

Lifestyle Intervention as the Primary Treatment for Pediatric Nonalcoholic Fatty Liver Disease

Weight loss is the most effective way to promote liver fat removal because it decreases the delivery of free fatty acids to the liver, increases extrahepatic insulin sensitivity, and reduces adipose tissue inflammation.

Dietary Manipulations for Nonalcoholic Fatty Liver Disease (NAFLD)

Pathophysiology of Nonalcoholic Fatty Liver Disease: Lifestyle-Gut-Gene Interaction

A variable interplay between the genetic background and the metabolic milieu is the likely physiopathologic mechanism involved in individual cases, which must be considered for implementing effective treatment strategies.

Nonalcoholic Fatty Liver Disease and Obesity Treatment

Diet and exercise that result in a sustained body weight reduction of 7–10% can improve liver fat content, NASH, and fibrosis, and more studies are needed before they can be recommended.

Dietary Composition Independent of Weight Loss in the Management of Non-Alcoholic Fatty Liver Disease

The potential therapeutic role of a “high quality healthy diet” to improve hepatic steatosis and metabolic dysfunction in patients with NAFLD, independent of caloric restriction and weight loss is highlighted.

Calorie-Restricted Mediterranean and Low-Fat Diets Affect Fatty Acid Status in Individuals with Nonalcoholic Fatty Liver Disease

The results indicate that dietary patterns and calorie restriction represent central therapeutic issues in the improvement of obesity-related cardiometabolic alterations that are involved in the mechanism of hepatic steatosis in NAFLD patients.

The Metabolic and Hepatic Impact of Two Personalized Dietary Strategies in Subjects with Obesity and Nonalcoholic Fatty Liver Disease: The Fatty Liver in Obesity (FLiO) Randomized Controlled Trial

The results support the benefit of energy-restricted diets, high adherence to the MedDiet, and high antioxidant capacity of the diet for the management of NAFLD in individuals with overweight or obesity.

How Much Fat Does One Need to Eat to Get a Fatty Liver? A Dietary View of NAFLD

In conclusion, a hypercaloric diet, independently of macronutrient composition, drives hepatic fat accumulation, whereas a few fat sources, in particular monounsaturated fatty acids and polyuns saturated fatty acids present in olive oil and fish, may reduce the risk of steatosis or even cure fatty liver.


A literature compilation evaluating the evidence behind dietary components, including calories intake, fat, protein, fibers and carbohydrate, especially fructose which could be a trigger to development and progression of the nonalcoholic fatty liver disease is provided.



A Pilot Randomised Study of the Metabolic and Histological Effects of Exercise in Non-alcoholic Steatohepatitis

Circuit exercise is safe and efficacious for improving cardiometabolic risk factors in patients with NAFLD, however this dose of circuit training, without concomitant weight loss, was insufficient for histological improvements in NAFLd.

Prospective histopathologic evaluation of lifestyle modification in nonalcoholic fatty liver disease: a randomized trial

Regardless of intervention group, lifestyle modification improved liver histology, as verified by repeat biopsy, after a 6-month intervention, which reinforces the importance of lifestyle modification as the primary treatment strategy for patients with NAFLD.

Behavior therapy for nonalcoholic fatty liver disease: The need for a multidisciplinary approach

The principles of behavior therapy are presented in detail, to help physicians change their prescriptive attitude into a more empowerment‐based approach and the practical aspects and public policies to be implemented at societal level to obtain the maximum effects in lifestyle changes.

Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease

In patients with NAFLD, daily fructose ingestion is associated with reduced hepatic steatosis but increased fibrosis, a readily modifiable environmental risk factor that may ameliorate disease progression in patients withNAFLD.

NAFLD incidence and remission: only a matter of weight gain and weight loss?

Alterations in adipose tissue and hepatic lipid kinetics in obese men and women with nonalcoholic fatty liver disease.

Obese persons with NAFLD have marked alterations in both adipose tissue and liver and hepatic TG metabolism, and fatty acids derived from nonsystemic sources are responsible for the increase in VLDL-TG secretion.

Randomized comparison of reduced fat and reduced carbohydrate hypocaloric diets on intrahepatic fat in overweight and obese human subjects

The decrease in intrahepatic lipids appears to be independent of visceral fat loss and is not tightly coupled with changes in whole body insulin sensitivity during 6 months of an energy restricted diet.

Randomized controlled trial testing the effects of weight loss on nonalcoholic steatohepatitis

Weight reduction achieved through lifestyle intervention leads to improvements in liver histology in NASH.