Fatty liver disease

The commonest liver disease in the world, and most people with it do not know

Fatty liver is fat accumulating inside liver cells in someone who does not drink heavily enough to explain it. It is extremely common — prevalence estimates in adults worldwide sit around a quarter to a third of the population, higher in people with type 2 diabetes or obesity — and it produces no symptoms until it is advanced.

It is also the condition most likely to be sitting quietly behind a metabolic panel that has come back "a bit off".

The name changed, twice

Worth knowing, because you will meet all three terms and may think they are different diseases.

• NAFLD — non‑alcoholic fatty liver disease. The old term, defined by what it is not.
• MAFLD — metabolic dysfunction‑associated fatty liver disease, proposed in 2020 to define it by what it is.
• MASLD — metabolic dysfunction‑associated steatotic liver disease, agreed by a multi‑society Delphi consensus in 2023, which is the current term. The inflamed form, previously NASH, became MASH.

The shift was partly about stigma and partly about accuracy: the condition is driven by metabolic dysfunction, and naming it after the absence of alcohol described the wrong thing.

The spectrum, and where it stops being reversible

1. Steatosis — fat in the liver, no significant inflammation. Common, and generally reversible.
2. Steatohepatitis (MASH) — fat plus inflammation and cell injury. This is the stage that can progress.
3. Fibrosis — scarring, in stages. The stage of fibrosis is the strongest predictor of long‑term outcome, more so than the amount of fat or inflammation.
4. Cirrhosis — advanced scarring, with the complications that follow.

Most people never move past the first stage. The clinical task is identifying the minority who are progressing, which is a different question from identifying who has fat in their liver.

Why liver enzymes are a poor screen

This is the part that catches people. A normal ALT does not exclude fatty liver, and does not exclude fibrosis. A substantial proportion of people with significant disease have enzymes in the normal range, because enzymes measure leakage from injured cells rather than the amount of fat or scar.

So a raised ALT is a useful prompt and a normal ALT is weak reassurance. Our baseline includes ALT because it is cheap and sometimes informative, not because it settles the question.

How it is actually assessed

• Ultrasound — widely available here, detects moderate to severe fat reasonably well, poor at mild fat, and does not stage fibrosis.
• FIB‑4 — a score calculated from age, AST, ALT and platelet count. Costs nothing beyond tests you may already have, and is recommended in several guidelines as the first‑line way to decide who needs more. Note it needs AST and platelets, which is one argument for adding AST when fatty liver is the question.
• Transient elastography — measures liver stiffness as a proxy for fibrosis. The usual next step where FIB‑4 is not reassuring.
• Biopsy — still the reference standard, now reserved for uncertain cases.

What is known to work

The evidence here is unusually concrete, and it is about weight rather than supplements.

Studies of weight loss in MASH have found a dose‑response relationship: modest loss improves liver fat, greater loss improves inflammation, and loss of around 10% of body weight was associated with improvement in fibrosis in a substantial share of participants. Fibrosis improving at all is notable, because scarring was long assumed to be one‑way.

Also supported: reducing alcohol regardless of the label on the disease, treating the associated diabetes, and physical activity, which improves liver fat even without much weight change.

Not supported: the liver‑cleansing supplements sold for this. Some of them raise liver enzymes themselves.

Why it matters in a metabolic clinic

Because it is the condition most likely to be present, least likely to be mentioned, and most responsive to the things being done anyway. It also travels with cardiovascular risk — people with MASLD more often die of heart disease than of liver disease.

The boundary

A raised ALT alongside central weight and high triglycerides is a reason to ask the question, not an answer. Whether you have this, at what stage, and what follows is a clinical assessment — and one worth making, because the early stages are among the few things in metabolic medicine that genuinely reverse.