Nonalcoholic Fatty Liver Disease: Nutritional Considerations

Obesity, diabetes, and insulin resistance syndrome are implicated in the genesis of nonalcoholic fatty liver diseases. These conditions involve steatosis and oxidative stress, both of which can be modulated by diet. Preliminary research suggests that weight reduction on a low–fat, high–fiber diet may be an effective treatment for NAFLD. Although further clinical trials are needed to establish the role of diet in treating these conditions, key nutritional issues are as follows: 

Weight Loss

Loss of excess weight may reduce the risk for NAFLD and effectively treat NASH. Compared with a rate of 20% in the general population, NAFLD affects up to 75% of obese individuals.² Gradual, moderate weight loss (~10% of body weight) usually reduces steatosis and may lead to improvement in liver function tests and histology.³ However, rapid weight loss exceeding ~1 lb per week in children and ~ 3.5 lbs per week in adults may result in necroinflammation, portal fibrosis, steatohepatitis, and bile stasis, along with worsening fibrosis.¹

Plant–based diets may be particularly helpful for both prevention and treatment of certain characteristic traits of NAFLD. Clinical trials have not yet evaluated the effect of low–fat, high–fiber vegetarian diets on NAFLD, as they have for cardiovascular disease and diabetes. However, these diets typically cause weight loss⁴ and can lower the concentrations of blood fats (eg, triglycerides) that contribute to nonalcoholic fatty liver disease.⁵ Such diets are also associated with reduced insulin resistance, another symptom of NAFLD,⁶ and greater antioxidant protection, compared with omnivorous diets.^7,8

In addition, iron accumulation aggravates insulin resistance and oxidative stress. Plant–based diets have somewhat less iron bioavailability, and vegetarians have lower body–iron stores.⁹

Alcohol Avoidance

Alcohol intake strongly predicts blood triglyceride concentrations, and dyslipidemias (including elevated triglycerides) are present in a majority of individuals with nonalcoholic fatty liver disease.¹⁰ Some evidence indicates that steatosis correlates directly with alcohol intake.¹¹ Consumption of more than 40 grams of alcohol per day doubles the risk of fatty liver¹² and other liver diseases. Women may be affected at even lower levels of intake (eg, 20–30 g/day). 

Two other nutritional issues merit mention:

Balanced Glucose and Lipid

Patients receiving total parenteral nutrition should receive a balanced ratio of glucose and lipid. Excess glucose administration (> 400 g/day for a 70–kg male) may cause steatosis through excessive hepatic lipogenesis. Patients receiving total parenteral nutrition should receive two thirds of nonprotein calories as glucose and one third as either long–chain triglycerides, or a mixture of medium–chain and long–chain triglycerides.¹³

Antioxidants

Some evidence suggests a role for dietary antioxidants. Oxidative stress, which is the imbalance between potentially harmful oxidants and protective antioxidants that are either diet–derived or endogenous, occurs in patients with fatty liver because of increased lipid oxidation.¹⁴ The result is depletion of ATP, DNA damage, alterations in protein stability, destruction of membranes via lipid peroxidation, and the release of proinflammatory cytokines.¹⁴ However, clinical trials have not been performed to determine the benefit of dietary or supplementary antioxidants in the prevention or treatment of this disease

Orders

See Basic Diet Orders chapter.

What to Tell the Family

In many cases fatty liver disease is responsive to diet changes, along with medications that address the elevations in weight, blood fats, and insulin resistance associated with this condition. Family members can assist the patient by participating in and encouraging a low–fat, high–fiber diet suitable for safe and gradual weight loss, along with appropriate exercise. These measures may help the patient avoid more serious liver damage.