Fatty liver disease is silent in nearly a third of adults

Nearly one in three adults worldwide carries excess fat in the liver, and most of them have no idea, because the disease produces no symptoms until scarring is already advanced. Danish hepatologist Aleksander Krag, a former president of the European liver societies, breaks down what steatotic liver disease actually is, why it was renamed in 2023, and which single number best predicts real risk.

From fatty liver to steatotic liver disease

For decades doctors called this condition fatty liver disease, then non-alcoholic fatty liver disease. In 2023 liver societies retired both terms. Fatty carries stigma in most languages, and non-alcoholic defines a disease by what it is not, which frustrates patients who don't drink at all. The new umbrella term is steatotic liver disease, from steatosis, the medical word for fat in the liver. A liver counts as steatotic once more than 5% of its weight is fat, visible on an ultrasound, CT scan, biopsy, or fibroscan.

Underneath that umbrella sit three subtypes, defined by what is driving the fat:

• MASLD (metabolic dysfunction associated steatotic liver disease): low alcohol intake, under roughly 20 to 30 grams a day, driven by obesity, type 2 diabetes, and other metabolic risk factors.
• MetALD: a mix of metabolic dysfunction and moderate alcohol, between roughly 30 and 50 to 60 grams a day.
• ALD (alcohol related liver disease): more than 50 to 60 grams of alcohol a day as the main driver.

Krag stresses that biology is not fixed. People move between these categories as their weight, diabetes control, or drinking habits change over time.

Why so many cases go unnoticed

Steatotic liver disease produces no symptoms until it reaches an advanced stage, when fluid accumulates in the abdomen, patients vomit blood from enlarged esophageal vessels, or toxins reach the brain and cause confusion, a condition called hepatic encephalopathy. By then the liver has often lost the reserve capacity it needs to compensate.

Krag frames this through Henry, a patient who arrived at the hospital decades into undiagnosed liver disease, too sick for a transplant. That case reshaped Krag's career toward early detection: finding people like Henry ten to fifteen years earlier, when lifestyle changes and new drugs can still change the outcome.

Fibrosis, not fat, is the number that matters

Fat inside the liver is dynamic. It can appear after a few days of heavy drinking and disappear once someone stops or loses weight. Fibrosis, the scarring that builds up between liver cells, is more stable, and it is the real driver of clinical disease. Without fibrosis, Krag argues the liver itself is usually not the biggest problem, obesity and type 2 diabetes are.

Disease typically advances one fibrosis stage roughly every seven years. Adding heavy alcohol use can cut that to about three years.

How doctors screen for it

Screening usually starts with FIB-4, a free index combining age, liver enzymes, and platelet count, recommended for anyone with type 2 diabetes, severe obesity, or persistently elevated liver enzymes. A high score leads to a confirmatory test such as fibroscan or elastography, technology originally developed to measure the ripeness of cheese in France, which measures liver stiffness through ultrasound or MRI.

A single, simple, at-home measurement also carries strong predictive value: abdominal circumference. Central obesity around the waist tracks much more closely with liver risk than body mass index alone.

Alcohol, underreported more than people think

The World Health Organization considers no amount of alcohol fully safe for the liver, and risk rises in an almost linear fashion, more steeply for women than men. Krag's research measured phosphatidylethanol, a blood metabolite of alcohol, in patients believed to have purely metabolic disease. Up to 38% of them actually drank enough to belong in the MetALD or ALD categories, evidence that self-reported drinking significantly underestimates real intake.

Everyday habits that move the needle

A randomized trial Krag's team ran found that a low carb, high fat diet reduced liver fat more than a standard diabetes diet, though patients who stopped dietician support often regained the fat. Coffee, interestingly, shows up consistently across decades of studies as protective for the liver, through a mechanism that remains unclear. Fruit deserves a caveat too: its fructose converts directly into liver fat, so Krag recommends not stacking every daily fruit and vegetable serving into apples and oranges alone. Smoking independently raises fibrosis risk and should stop regardless of drinking habits.

Where drug treatment is heading

Semaglutide, a GLP-1 receptor agonist, and resmetirom became the first two drugs conditionally approved by the FDA and EMA for MASH with significant fibrosis, used alongside diet and exercise. In phase three trials, semaglutide reduced fibrosis after 72 weeks of treatment, evidence of a direct liver effect beyond weight loss alone. Resmetirom works differently, correcting a localized hypothyroid-like state inside liver cells. A newer class of drugs, FGF21 analogs, is now in phase three trials and has shown early signals of reversing cirrhosis in advanced disease, a result Krag calls genuinely exciting for patients who previously had few options.

The takeaway

For anyone in their 30s or 40s who drinks socially and carries some extra weight, Krag's advice is concrete: count how many drinks you actually have each week, give the liver alcohol-free days, and ask a doctor for a FIB-4 test alongside routine diabetes or obesity checkups. Fibrosis is reversible at nearly every stage if it's caught early enough, which makes finding it the single highest-leverage step most people can take.