Steatosis is the medical term for fat buildup in the liver. It’s defined by the presence of visible fat droplets in more than 5% of liver cells. Most people with steatosis have no symptoms at all, and the condition is typically discovered by accident during blood work or imaging done for something else. While steatosis on its own is generally not dangerous, it can progress to more serious liver disease if the underlying cause isn’t addressed.
How Fat Accumulates in the Liver
Your liver normally processes fat as part of its daily work. It takes in fatty acids from your bloodstream, uses some for energy, converts some into other molecules, and packages the rest into particles that get shipped back out into the blood. Steatosis develops when this system falls out of balance: the liver either takes in too much fat, produces too much fat internally, burns too little of it for energy, or can’t export it fast enough. When any combination of these problems persists, triglycerides (a common type of fat) start piling up inside liver cells as lipid droplets.
Pathologists grade steatosis on a simple scale based on how many liver cells are affected. Grade 0 means fewer than 5% of cells contain fat (essentially normal). Grade 1 covers 5% to 33%, grade 2 covers 34% to 66%, and grade 3 means more than two-thirds of liver cells are storing excess fat.
Two Patterns Under the Microscope
When a liver biopsy is examined, fat accumulation shows up in one of two patterns. In macrovesicular steatosis, a single large fat droplet fills the cell and pushes the nucleus to the edge. This is the most common form seen in people with metabolic or alcohol-related fatty liver disease. On its own, macrovesicular steatosis has a generally good long-term outlook and rarely progresses to scarring or cirrhosis without other contributing factors.
Microvesicular steatosis looks quite different. The cell fills with many tiny fat droplets (each less than one micrometer across), giving the cell a foamy appearance, with the nucleus staying in the center. When it appears as a widespread, diffuse pattern, microvesicular steatosis signals a more urgent problem. It’s linked to conditions like acute fatty liver of pregnancy, Reye syndrome, and certain drug toxicities, all of which involve severe disruption of the cell’s ability to burn fat for energy. In the context of chronic fatty liver disease, patches of microvesicular steatosis are associated with more advanced cell damage and scarring.
Symptoms and How It’s Found
Steatosis is a silent condition. Most people feel completely normal. When symptoms do appear, they’re vague: fatigue or mild discomfort in the upper right part of the abdomen. A doctor might suspect fatty liver after noticing elevated liver enzymes on routine blood work, an enlarged liver during a physical exam, or a bright-appearing liver on an ultrasound or CT scan ordered for an unrelated reason.
The most precise noninvasive way to measure liver fat is a specialized MRI technique called MRI-PDFF (proton density fat fraction), which detects steatosis at the 5% fat threshold. Ultrasound-based tools can also estimate liver fat, though they’re somewhat less accurate. CT scans can show fatty liver but involve radiation and don’t quantify fat reliably. A liver biopsy remains the definitive way to assess not just fat content but also inflammation and scarring, though it’s reserved for cases where more detail is needed.
What Causes It
The most common cause, by far, is metabolic. Excess body weight, insulin resistance, type 2 diabetes, and high triglyceride levels all drive fat accumulation in the liver. This form was long called nonalcoholic fatty liver disease (NAFLD) but was renamed in 2023 to metabolic dysfunction-associated steatotic liver disease, or MASLD. Globally, roughly 15% of the population had MASLD as of 2021, up from about 12% in 1990. Rates are highest in North Africa and the Middle East and have been climbing fastest in Western Europe.
Alcohol is the other major driver. Heavy or prolonged drinking overwhelms the liver’s fat-processing capacity in much the same way metabolic dysfunction does, leading to alcohol-associated steatosis.
Several medications can also trigger steatosis as a side effect. Amiodarone (a heart rhythm drug) interferes with fat burning inside liver cells. Methotrexate (used for autoimmune conditions and some cancers) disrupts energy production in cells. Corticosteroids promote weight gain and insulin resistance while simultaneously slowing the liver’s ability to break down and export fat. Rarer causes include certain genetic conditions that impair the liver’s fat-export machinery.
Why the Name Changed From NAFLD to MASLD
In 2023, a global consortium of liver specialists formally replaced the term NAFLD with MASLD. The change happened for several reasons. The old name defined the disease by what it wasn’t (nonalcoholic) rather than what it was, which didn’t reflect what scientists had learned about its metabolic roots. The terms “nonalcoholic” and “fatty” were also considered stigmatizing. In surveys of the medical community, roughly 61% and 66% of respondents found those terms potentially harmful to patients, respectively.
There was a practical problem, too. NAFLD excluded anyone who drank even moderate amounts of alcohol, which meant many patients with clear metabolic liver disease were left out of clinical trials and research efforts, even though they were at higher risk for poor outcomes. The new framework uses “steatotic liver disease” as a broad umbrella, then sorts patients into more specific categories: MASLD for those with metabolic risk factors, alcohol-associated liver disease for heavy drinkers, and overlapping categories for people who have both.
When Steatosis Becomes More Serious
Simple steatosis (fat without inflammation) is the earliest and most benign stage. The concern is what comes next. In some people, the liver becomes inflamed, a condition now called metabolic dysfunction-associated steatohepatitis (MASH, formerly NASH). This inflammatory stage is what drives scarring, and eventually, cirrhosis.
Scientists initially described this progression as a “two-hit” process: first fat accumulates, then a second insult triggers inflammation. The current understanding is more complex. Multiple factors act simultaneously: signals from excess body fat, changes in gut bacteria that allow inflammatory molecules into the bloodstream, stress within liver cells themselves, and a buildup of cellular danger signals over time. Not everyone with steatosis progresses. Many people live with stable fat accumulation for decades without developing significant inflammation or scarring.
Reversing Liver Fat
The encouraging news is that steatosis is reversible. Weight loss is the most effective intervention. Losing 7% to 10% of your body weight through a combination of dietary changes, increased physical activity, and behavioral modification reliably reduces liver fat and improves liver function tests. A 10% reduction in body weight has been shown to cut liver fat content by 44% to 58% in overweight adults. Gradual weight loss, no more than about 1.6 kilograms (3.5 pounds) per week, is recommended to avoid stressing the liver further.
No specific diet is required, though reducing sugar, refined carbohydrates, and alcohol all help lower the liver’s fat burden. For people whose steatosis is caused by a medication, switching to an alternative drug (when possible) can resolve the problem. When alcohol is the driver, reducing or eliminating intake allows the liver to clear accumulated fat, often within weeks to months.
For people who have progressed beyond simple steatosis into active inflammation or early scarring, the same weight loss targets apply, though the urgency is greater. Newer medications specifically targeting MASH are beginning to become available, but lifestyle changes remain the foundation of treatment at every stage.