Non-alcoholic fatty liver disease (NAFLD)

Disease Definition and Causes

Non-alcoholic fatty liver disease (NAFLD) is a non-inflammatory disorder characterized by clinical and histological changes in the liver structure, such as excess accumulation of fat molecules (triglycerides) in liver cells (hepatocytes), fatty inflammation, tissue softening, and liver scarring. Other terms for the disease include “fatty liver” and “fatty degeneration of the liver.”

NAFLD has a relatively benign course, but its close association with several metabolic disorders increases the risk of developing complications in the heart and blood vessels, affecting the patient’s prognosis and reducing their quality and length of life.

Accumulation of fat molecules in liver cells leads to the destruction of cell membrane structures, altering oxidation processes and substance exchange within them. As a result, affected cells break down, fibrotic tissues (scar tissue) form in their place, impairing liver function, which in turn causes changes in blood composition, increases the risk of developing metabolic syndrome, and leads to the formation of cirrhotic changes in the organ.

Non-alcoholic fatty liver disease can develop in anyone aged 30 and older who does not abuse alcohol but regularly consumes small amounts, prefers calorie-rich fatty foods, and leads a sedentary lifestyle. Although the disease in most cases progresses approximately or completely asymptomatic, structural changes in the organ advance, exacerbating metabolic disturbances, reflected in additional test results. The prevalence of the disease worldwide is estimated to be around 20%.

Types of non-alcoholic fatty liver disease are classified into 4 grades (stages) based on the amount of fat deposits in liver cells:

  • Grade 0: Small fat droplets appear on the surface of some hepatocytes individually.
  • Grade I: Medium and large fat droplets are superficially concentrated on small functional cell clusters in the organ.
  • Grade II: Hepatocytes saturate with triglycerides and accumulate inside.
  • Grade III: Fat affects the structural tissue of the organ rapidly across its entire surface, accumulates in the intercellular space, and forms cysts.

Depending on the causes of disease development, non-alcoholic fatty liver disease can be either primary (resulting from metabolic syndrome) or secondary (resulting from the toxic effects of external factors on the liver, such as harmful medication intake, surgical procedures on the digestive organs, and prolonged fasting).

In the initial stage of the disease process, no external symptoms appear. It is discovered incidentally during preventive examinations or when visiting a doctor for another illness. NAFLD is characterized by active renewal, so the functional capacities of the organ remain alive for a long period from the onset of the disease.

Over time, the function of damaged cells decreases, and symptoms of non-alcoholic fatty liver disease appear:

  • Feeling of heaviness and discomfort in the lower right side and upper middle area.
  • Nausea.
  • Belching.
  • Metallic taste in the mouth.
  • General weakness, fatigue, and decreased ability to work.
  • Weight gain.
  • Unexplained fever.
  • Appearance of spider veins on the skin.

In case of significant disease progression and development of complications, jaundice may occur in the skin, eyes, and mucous membranes, itching of the skin, and presence of fluid in the abdomen (ascites).

The causes of non-alcoholic fatty liver disease include an unhealthy lifestyle and the body’s involvement in lipid metabolism disorders. Contributing factors include:

  • Abdominal obesity (waist circumference over 80 cm for women and 94 cm for men).
  • Digestive system diseases (hyperthyroidism, Cushing’s syndrome).
  • Glucose intolerance, non-exercise diabetes.
  • Unbalanced nutrition.
  • Parenteral nutrition (intravenous injection of nutrient solutions).
  • Acute and chronic viral hepatitis.
  • Congenital liver abnormalities and genetic deficiency of enzymes involved in fat metabolism.
  • Sedentary lifestyle.
  • High blood pressure.
  • Consumption of certain medications (amiodarone, corticosteroids).

Diagnosing non-alcoholic fatty liver disease (NAFLD) relies heavily on gathering patient complaints, medical history, and assessing potential risk factors. Before confirming this diagnosis, other liver diseases, especially those arising from viral origins, must be ruled out. Necessary methods for evaluating suspected NAFLD patients include:

  • Complete blood count and urinalysis.
  • Fibrosis degree testing.
  • Blood clotting analysis.
  • Chemical blood analysis (alanine aminotransferase, aspartate aminotransferase, cholesterol, total and fractional bilirubin, alkaline phosphatase, glucose, protein fraction).
  • Blood testing for infection (determining signs of viral hepatitis).
  • Liver biopsy with histological analysis of the sample taken.
  • Ultrasound examination of the liver and gallbladder.
  • Computer and magnetic resonance imaging of the liver.
  • Elasticity measurement (elastometry).

These tests and examinations collaborate to provide an accurate assessment of liver condition and determine the extent of non-alcoholic fatty liver disease impact.


Primarily, lifestyle improvement is considered the key element in treating NAFLD. This involves engaging in physical activity for at least 150 minutes per week, maintaining body weight within the normal range, avoiding alcohol consumption and certain medications, following a balanced diet, and adhering to a healthy lifestyle.

Patients should exclude fatty meats, fish, canned foods, smoked products, easily digestible carbohydrates, cooking fats, chocolate and ice cream, cocoa, black coffee, and alcohol from their diet. It is preferable to consume low-fat meats and fish, vegetables and fruits, and complex carbohydrates (whole grains and pasta varieties).

The optimal weight loss rate in cases of fatty liver disease is 1 kg per 7 days. Rapid weight loss can lead to the development of fat accumulation, fatty liver inflammation, and accelerated liver tissue fibrosis. Reducing the weight of individuals suffering from obesity and non-alcoholic fatty liver disease by 10% results in a significant improvement in liver enzyme levels such as AST and ALT, as well as tissue indicators.

Pharmacological treatment includes:

  • Medications to improve insulin resistance.
  • Omega-3 fatty acids, statins, fibrates to reduce the risk of cardiovascular complications.
  • Hepatoprotective agents.

In cases where other alleviation methods are ineffective, bariatric surgery (gastric bypass) can be considered – procedures redirecting and narrowing the stomach.

Progressive deterioration of liver function may indicate the need for liver transplantation.

Prevention of non-alcoholic fatty liver disease:

To reduce the risk of developing NAFLD, it is preferable to:

  • Engage in physical activity and avoid a sedentary lifestyle.
  • Monitor and maintain weight within normal values, avoiding obesity.
  • Consume a healthy diet (the Mediterranean diet is an ideal choice).
  • Undergo regular preventive examinations and tests to detect cardiovascular, digestive system, and liver diseases early.

These measures aim to improve lifestyle and prevent factors that increase the risk of developing non-alcoholic fatty liver disease.

  1. Clinical guidelines on the diagnosis and treatment of non-alcoholic fatty liver disease, as outlined by the Russian Society for the Study of the Liver and the Russian Gastroenterological Association. Published in the Hepatology Journal (Issue 2, 2016, pages 24-42).
  2. Bueverov, A.O., Bogomolov, P.O., Maevskaya, M.V. Exploring pathogenetic treatments for non-alcoholic steatohepatitis: examining rationale, effectiveness, and safety. Appearing in the Therapeutic Archive (2007), Volume 79, Issue 8, with details on pages 1-4.
  3. Lazebnik, L.B., Radchenko, V.G., Golovanova, E.V., et al. Insights into non-alcoholic fatty liver disease: covering clinical features, diagnosis, and treatment. Featured in Experimental and Clinical Gastroenterology — Moscow, 2015. This comprehensive review spans from pages 85 to 96.