NAFLD, or nonalcoholic fatty liver disease, is a condition where excess fat builds up in the liver of people who drink little to no alcohol. It affects roughly one in four adults worldwide, making it the most common chronic liver condition on the planet. The name itself is now being phased out in favor of a newer term, but the condition and its consequences remain the same.
How Fat Builds Up in the Liver
A healthy liver contains some fat, but problems start when fat makes up more than 5% of the liver’s weight. The process is closely tied to how your body handles insulin. When cells become resistant to insulin, two things happen at once: fat tissue starts releasing more fatty acids into the bloodstream, and the liver ramps up its own fat production. Those fatty acids flood into the liver faster than it can process or export them, so they accumulate.
At the same time, elevated insulin and blood sugar levels interfere with the liver’s ability to burn fat for energy. The result is a feedback loop: the liver takes in more fat, makes more fat, and breaks down less of it. Over time, fat droplets fill liver cells and the organ becomes visibly fatty on imaging scans.
Simple Fatty Liver vs. NASH
NAFLD exists on a spectrum. The earliest and most common form is simple steatosis, sometimes called NAFL. In this stage, fat is present but the liver cells aren’t significantly damaged. Most people with simple fatty liver never develop serious liver problems.
The more concerning form is NASH (nonalcoholic steatohepatitis). What separates NASH from simple fatty liver is active cell damage: liver cells swell and “balloon,” and inflammation sets in. This ballooning degeneration is the hallmark feature that distinguishes NASH on a biopsy. Over years or decades, the repeated cycle of inflammation and repair can produce scar tissue (fibrosis), which may eventually progress to cirrhosis or liver cancer in a subset of patients. Roughly 10% to 25% of people with NAFLD develop NASH.
Risk Factors Beyond Weight
Obesity, type 2 diabetes, high blood pressure, and high triglycerides are the most well-known risk factors. But not everyone with fatty liver fits that profile. Genetics play a meaningful role. A variant of the PNPLA3 gene (known as the G allele of rs738409) triples the odds of developing NAFLD and drives increasingly severe liver damage. Notably, this genetic risk operates independently of body weight, cholesterol levels, or diabetes. People who carry it can develop significant liver fat accumulation without the typical metabolic warning signs, which means fatty liver sometimes shows up in people who wouldn’t otherwise be screened for it.
Ethnicity also matters. Hispanic populations carry the PNPLA3 risk variant at higher rates, which partly explains observed differences in NAFLD prevalence across ethnic groups. Other contributing factors include a sedentary lifestyle, diets high in refined carbohydrates and sugary drinks, and certain medications that promote fat storage in the liver.
How NAFLD Is Diagnosed
NAFLD is often discovered incidentally when blood work shows elevated liver enzymes or an imaging scan reveals a bright, fatty liver. To qualify as NAFLD rather than alcohol-related liver disease, daily alcohol intake must be below 30 grams for men and 20 grams for women (roughly two standard drinks and one and a half drinks, respectively).
A FibroScan is one of the most common noninvasive tools used to assess both fat content and scarring. It produces two scores. The CAP score measures fat: 238 to 260 dB/m indicates 11 to 33% fatty change (grade S1), 260 to 290 dB/m indicates 34 to 66% (grade S2), and anything above 290 dB/m means 67% or more of the liver is affected (grade S3). The stiffness score estimates fibrosis. A liver biopsy remains the definitive way to confirm NASH and assess fibrosis stage, but it’s typically reserved for cases where the diagnosis would change treatment decisions.
Cardiovascular Disease Is the Biggest Threat
This surprises many people: the leading cause of death in NAFLD patients is not liver failure. It’s cardiovascular disease. The same insulin resistance and metabolic dysfunction that drives fat into the liver also accelerates plaque buildup in arteries. A large meta-analysis of over 25,000 patients found that NAFLD raised the risk of cardiovascular events by 77% and cardiovascular death by 43%, according to the American Heart Association. Some individual studies have reported even higher numbers depending on the population studied.
This means that managing NAFLD isn’t just about protecting the liver. It’s about addressing the full constellation of metabolic risks, including blood pressure, blood sugar, and cholesterol.
Weight Loss Is the Most Effective Treatment
No amount of medication replaces what weight loss can do for a fatty liver. Losing 7 to 9% of your body weight through diet, exercise, and behavioral changes improves liver enzyme levels and reduces fat accumulation. Reaching a 10% loss is even more powerful, cutting liver fat content by 44 to 58% in overweight adults and improving the inflammatory and scarring changes seen in NASH. The recommended pace is no more than 1.6 kilograms (about 3.5 pounds) per week, since rapid weight loss can paradoxically worsen liver inflammation.
The type of diet matters less than the calorie deficit, though most liver specialists encourage a Mediterranean-style eating pattern rich in vegetables, whole grains, fish, and olive oil while limiting added sugars and refined carbohydrates. Regular physical activity helps even when the number on the scale doesn’t move much, because exercise independently improves insulin sensitivity and reduces liver fat.
The First Medication for NASH
In 2024, the FDA approved the first medication specifically for NASH with moderate to advanced liver scarring. In a phase 3 trial published in the New England Journal of Medicine, the drug achieved NASH resolution without worsening fibrosis in about 26 to 30% of patients (compared to roughly 10% on placebo) and improved fibrosis by at least one stage in about 24 to 26% of patients (compared to 14% on placebo). These numbers represent a real but modest benefit, and the drug is intended for people with significant fibrosis, not everyone with fatty liver.
The Name Is Changing to MASLD
In 2023, international liver disease organizations formally renamed NAFLD to MASLD, or metabolic dysfunction-associated steatotic liver disease. NASH became MASH (metabolic dysfunction-associated steatohepatitis). The change happened for several reasons. The term “nonalcoholic” defined the disease by what it wasn’t rather than what caused it, and surveys found that a majority of both patients and clinicians considered the words “nonalcoholic” and “fatty” stigmatizing.
The new criteria also shift MASLD from a diagnosis of exclusion to one based on specific criteria. To be diagnosed with MASLD, you need evidence of liver fat plus at least one of five cardiometabolic risk factors, such as elevated blood sugar, high blood pressure, or excess waist circumference. A new category called MetALD was created for people who have both metabolic risk factors and moderate alcohol consumption (more than 140 grams per week for women, 210 grams for men). You’ll see both sets of terms used in medical settings during the transition period, but they describe the same underlying disease.