Non-Alcoholic Fatty Liver Disease (NAFLD): An Overview

Introduction

Non-Alcoholic Fatty Liver Disease (NAFLD) is among the most common liver conditions worldwide, affecting roughly one-quarter of the global population. It spans a spectrum from simple steatosis (fat accumulation) to non-alcoholic steatohepatitis (NASH), which adds inflammation and hepatocellular injury and may progress to fibrosis, cirrhosis, and hepatocellular carcinoma. NAFLD is tightly linked to metabolic risk factors such as obesity, type 2 diabetes, dyslipidemia, and hypertension (the metabolic syndrome).

Epidemiology

Prevalence has risen in step with global increases in obesity and insulin resistance. In many Western countries, an estimated 30–40% of adults have some degree of NAFLD. Pediatric and adolescent cases are also increasing, mirroring dietary patterns and sedentary lifestyles.

Diagnosis

Evaluation often begins after incidental abnormal liver enzymes or imaging. Exclude significant alcohol intake and secondary causes (viral hepatitis, medications, other liver diseases). Common steps:

• Laboratory tests: ALT/AST, bilirubin, albumin, INR; metabolic profile.
• Ultrasound: First-line imaging to detect hepatic steatosis.
• CT/MRI: Additional characterization when needed.
• Liver biopsy: Gold standard to distinguish NASH from simple steatosis and stage fibrosis when noninvasive tests are inconclusive.

Treatment

Lifestyle modification is foundational; medications may be considered in selected patients.

• Dietary changes: Balanced, calorie-appropriate eating patterns emphasizing vegetables, fruits, whole grains, lean proteins, and healthy fats.
• Physical activity: Regular aerobic exercise and resistance training support weight reduction and improve liver enzymes.
• Weight loss: Even modest reduction can improve steatosis; greater loss is associated with improved inflammation and fibrosis.
• Pharmacotherapy (selected cases): Agents such as vitamin E, pioglitazone, or diabetes therapies may be considered in patients with NASH or advanced fibrosis, based on clinician guidance.
• Risk factor control: Address diabetes, dyslipidemia, hypertension, and sleep apnea to reduce overall cardiometabolic risk.

Future Directions

Research continues on antifibrotic and anti-inflammatory therapies and on improved noninvasive tools for diagnosis and staging. Genetic and metabolic profiling are also being studied to better predict disease susceptibility and progression.

Conclusion

NAFLD is a growing public health concern. Early identification, lifestyle modification, and management of metabolic risks are central to preventing progression to NASH, advanced fibrosis, cirrhosis, and hepatocellular carcinoma.

References

1. Younossi Z, Anstee QM, Marietti M, et al. Global burden of NAFLD and NASH. Nat Rev Gastroenterol Hepatol. 2018;15(1):11-20.
2. Friedman SL, Neuschwander-Tetri BA, Rinella M, Sanyal AJ. Mechanisms and therapeutic strategies. Nat Med. 2018;24(7):908-922.
3. Chalasani N, Younossi Z, Lavine JE, et al. AASLD practice guidance for NAFLD. Hepatology. 2018;67(1):328-357.

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