Fatty liver disease, known medically as hepatic steatosis, is a build-up of fat in the liver. It affects about one adult in three worldwide, usually without any symptoms. Since 2023, its most common form has been called MASLD, a name that highlights its link with excess weight, diabetes and blood pressure. At an early stage, it can be reversed.
Key points
- Metabolic fatty liver disease (MASLD) affects about 30% of adults worldwide and 18.3% of adults with no other liver disease in the French Constances cohort.
- It is not the fat itself that determines the outlook but fibrosis: the risk of liver-related death rises sharply with its stage.
- Among 293 patients followed for a year, steatohepatitis had resolved in 90% of those who lost at least 10% of their body weight.
- No supplement has an authorised claim for fatty liver; only choline has a claim relating to liver function.
What is fatty liver disease and what does MASLD mean?
In 2023, three major international scientific societies replaced the former term NAFLD (non-alcoholic fatty liver disease) with MASLD, short for metabolic dysfunction-associated steatotic liver disease. The diagnosis requires fat in the liver plus at least one of five cardiometabolic risk factors: excess weight or a large waist, raised blood sugar or type 2 diabetes, raised blood pressure, raised triglycerides, or low HDL cholesterol. Excessive alcohol consumption must also be ruled out.
An intermediate category, MetALD, covers people who have these metabolic factors and drink more: 140 to 350g of alcohol per week for women, 210 to 420g for men. What used to be called NASH is now called MASH.
Steatosis, steatohepatitis, fibrosis: what are the stages?
The disease may or may not progress, in stages:
- simple steatosis: fat without significant inflammation;
- steatohepatitis (MASH): the fat comes with inflammation and damage to liver cells (hepatocytes);
- fibrosis: scar tissue forms, graded from F0 (none) to F4;
- cirrhosis (F4), which carries a risk of complications and liver cancer.
Most people never get beyond simple steatosis: the point of follow-up is to detect fibrosis.
Who gets fatty liver disease?
A great many people. A meta-analysis of 92 studies covering more than 9 million people puts global prevalence at 30% over 1990-2019, and rising: 25% in 1990-2006, 38% in 2016-2019. Western Europe sits at around 25%.
In France, in the Constances cohort (137,206 adults), 18.3% of participants with no other liver disease had steatosis estimated by an index (weight, waist size, triglycerides, gamma-GT), and 2.7% of them had probable advanced fibrosis. These people had more liver, cardiovascular and kidney complications.
What causes fatty liver?
The main cause is metabolic: when cells respond poorly to insulin, the liver receives more fatty acids and makes more fat from sugars (see our article on insulin resistance). Contributing factors:
- excess weight, especially abdominal fat, and type 2 diabetes;
- a sedentary lifestyle and a diet high in added sugars and ultra-processed foods;
- alcohol, which tips the picture towards MetALD or alcohol-related liver disease;
- more rarely, certain medicines or a lack of choline: in four patients fed intravenously without choline, the steatosis disappeared after six weeks of intravenous choline.
What are the symptoms of fatty liver?
Most often, none. Fatty liver is usually found by chance, on an ultrasound scan or on a blood test showing slightly raised transaminases (ALT, AST) or gamma-GT. Tiredness or discomfort under the right ribs is sometimes reported, but is not specific. Normal transaminases do not rule out fatty liver.
How is fatty liver diagnosed?
The 2024 European guidelines (EASL-EASD-EASO) focus mainly on detecting fibrosis, step by step, in people at risk: type 2 diabetes, obesity with another metabolic factor, abnormal liver enzymes, or steatosis seen on imaging.
| Test | What it measures | When it is used |
|---|---|---|
| Liver ultrasound | The presence of fat (a “bright” liver) | Often the test that first detects fatty liver |
| Liver function tests (ALT, AST, gamma-GT) | Damage to liver cells | Baseline check; may be normal |
| FIB-4 score | A fibrosis risk, calculated from age, transaminases and platelets | First step to rule out advanced fibrosis |
| Transient elastography | Liver stiffness, which reflects fibrosis | Second step if the FIB-4 is not reassuring |
| Liver biopsy | Inflammation and the exact fibrosis stage | Rarely, when in doubt |
An ultrasound report describing “mild”, “moderate” or “severe” steatosis refers to the amount of fat, not to fibrosis: only a fibrosis assessment tells you how serious it is.
Is fatty liver disease serious?
It is rarely serious in itself, but it signals a background that needs watching. A meta-analysis of five cohorts (1,495 patients followed over 17,452 patient-years) shows that mortality rises with fibrosis stage. Compared with no fibrosis, the risk of death from any cause is multiplied by 1.6 at stage F1, 2.5 at stage F2, 3.5 at stage F3 and 6.4 at stage F4. The risk of liver-related death rises even faster.
For most people with fatty liver, the main risk remains cardiovascular: blood pressure, cholesterol and blood sugar are part of the management.
Can fatty liver be reversed?
Yes, especially before the cirrhosis stage. The best-documented levers are weight loss, physical activity, diet, and stopping or sharply reducing alcohol.
How much weight should you aim to lose?
In a study carried out in Havana, 293 patients with biopsy-proven steatohepatitis followed lifestyle advice for 52 weeks, with a follow-up biopsy. The results depended clearly on the weight lost:
- with at least 5% of body weight lost, steatohepatitis resolved in 58% of patients;
- with at least 10%, it resolved in 90% of them, and fibrosis regressed in 45%.
Only 30% of participants reached 5%: the goal requires support.
Does physical activity work without weight loss?
Partly, yes. A meta-analysis of 12 controlled trials measured a reduction in liver fat with regular exercise, even with minimal or no weight loss, and at volumes below those recommended for weight loss. The effect on transaminases was not significant. The trials tested aerobic exercise, resistance training or both.
What should you eat if you have fatty liver?
The most widely recommended pattern is the Mediterranean diet: vegetables, pulses, wholegrains, fish, olive oil, nuts, and fewer sugars and refined flours. According to a key review, it can reduce liver fat even without weight loss. In practice:
- limit sugary drinks, desserts and ultra-processed foods;
- choose unsaturated fats (olive oil, oily fish, nuts);
- cut right down on alcohol, which worsens the disease at every stage.
“Detox” programmes have no solid basis: our article liver detox, myth or reality looks at the evidence.
Is coffee good for the liver?
A meta-analysis of five studies linked regular coffee drinking with a 29% lower risk of fatty liver and, in people who have it, a 30% lower risk of fibrosis. These are observational studies: they show an association, not a proven effect.
Are there medicines for fatty liver disease?
Yes, recently and depending on the country, for steatohepatitis with fibrosis, on prescription. In a phase 3 trial (966 patients, 52 weeks), resmetirom resolved steatohepatitis in 26 to 30% of patients, compared with 10% on placebo. Semaglutide, a treatment for diabetes and obesity, achieved 62.9% resolution versus 34.3% (800 patients, 72 weeks), with an average weight loss of 10.5%. These medicines are not intended for simple steatosis.
Food supplements and fatty liver: what do the trials show?
No food supplement treats fatty liver, and no health claim is authorised in Europe for this use. The 2024 European guidelines put lifestyle first; the only targeted treatment they include is a medicine, resmetirom. Here is what the main trials show.
| Substance | Trial | Main result | Limitations |
|---|---|---|---|
| Vitamin E, 800IU per day | 247 non-diabetic adults with steatohepatitis (3 groups), 96 weeks | Improvement in steatohepatitis in 43% versus 19% on placebo | High dose, under medical advice; no effect on fibrosis |
| Silymarin (milk thistle), 700mg three times a day | 99 adults with steatohepatitis, 48 weeks | Primary endpoint not met (32.7% versus 26.0%); fibrosis reduced on biopsy in 22.4% versus 6.0% | Single centre, secondary result |
| Berberine, 0.5g three times a day | 184 patients (3 groups), 16 weeks, with lifestyle advice | Liver fat: −52.7% versus −36.4% with advice alone | Open-label trial, no placebo |
| Choline | 57 adults deprived of choline for up to 42 days, under controlled conditions | Fatty liver or muscle damage in 77% of men | Shows the effect of a deficiency, not the value of extra intake |
Vitamin E. This antioxidant targets the oxidative stress of steatohepatitis (see oxidative stress and antioxidants), but at a dose far above dietary intake, tested under medical supervision.
Silymarin. The milk thistle extract missed its primary endpoint; the signal on fibrosis remains to be confirmed (see our article on milk thistle). Black radish has, to our knowledge, only been tested on fatty liver in animals.
Berberine. Berberine interacts with several medicines: see the precautions in our article on berberine.
Choline. It is the only nutrient on this list with a claim relating to the liver: “Choline contributes to the maintenance of normal liver function”, as well as “Choline contributes to normal lipid metabolism”. These claims may only be used for a food providing at least 82.5mg of choline per 100g, 100ml or per serving. They do not concern fatty liver disease. Sources and requirements are covered in our article on choline.
Frequently asked questions
Can fatty liver be reversed?
Yes, in most cases, as long as fibrosis is not advanced. Liver fat decreases with weight loss, physical activity and a Mediterranean-style diet. Fibrosis can also regress, but more slowly and less often.
What is the life expectancy with fatty liver disease?
It depends mainly on the fibrosis stage and other risk factors, not on the amount of fat. The risk of death is lowest without fibrosis and rises with each stage, which is why the FIB-4 and elastography matter.
Which foods should you avoid with fatty liver?
Above all alcohol, sugary drinks, desserts and ultra-processed foods high in sugars and refined flours. It is the overall diet and weight loss that count, more than any single food.
Can you have fatty liver without being overweight?
Yes. A single one of the five cardiometabolic factors is enough for a diagnosis of MASLD: raised blood sugar, blood pressure or triglycerides, even without excess weight.
How long does it take to reduce fatty liver?
A few months. In the berberine trial, liver fat had already fallen at 16 weeks in both groups; in the Havana study, follow-up biopsies were done at 52 weeks. The pace depends mainly on weight loss.
Which doctor should you see for fatty liver?
Your GP carries out the initial assessment and calculates the FIB-4. They will refer you to a liver specialist (hepatologist or gastroenterologist) if fibrosis risk has not been ruled out, or in the case of very high enzymes, alcohol use or another liver disease.
Conclusion
Fatty liver disease is common, silent and often benign at first. What matters is the fibrosis stage, assessed with the FIB-4 and then elastography. The most solid levers are well known: losing 5 to 10% of body weight, moving regularly, eating a Mediterranean-style diet and cutting down on alcohol. No supplement treats fatty liver or replaces this follow-up.
Sources
- Rinella ME et al. (2023). A multisociety Delphi consensus statement on new fatty liver disease nomenclature. Journal of Hepatology, 79(6), 1542-1556. doi:10.1016/j.jhep.2023.06.003
- European Association for the Study of the Liver (EASL), European Association for the Study of Diabetes (EASD), European Association for the Study of Obesity (EASO) (2024). EASL-EASD-EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD). Journal of Hepatology, 81(3), 492-542. doi:10.1016/j.jhep.2024.04.031
- Younossi ZM et al. (2023). The global epidemiology of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH): a systematic review. Hepatology, 77(4), 1335-1347. doi:10.1097/HEP.0000000000000004
- Nabi O et al. (2023). The NAFLD burden on mortality and morbidities in general population: a community-based longitudinal study (NASH-CO study). Liver International, 43(10), 2096-2106. doi:10.1111/liv.15674
- Dulai PS et al. (2017). Increased risk of mortality by fibrosis stage in nonalcoholic fatty liver disease: systematic review and meta-analysis. Hepatology, 65(5), 1557-1565. doi:10.1002/hep.29085
- Vilar-Gomez E et al. (2015). Weight loss through lifestyle modification significantly reduces features of nonalcoholic steatohepatitis. Gastroenterology, 149(2), 367-378. doi:10.1053/j.gastro.2015.04.005
- Keating SE et al. (2012). Exercise and non-alcoholic fatty liver disease: a systematic review and meta-analysis. Journal of Hepatology, 57(1), 157-166. doi:10.1016/j.jhep.2012.02.023
- Romero-Gómez M, Zelber-Sagi S, Trenell M (2017). Treatment of NAFLD with diet, physical activity and exercise. Journal of Hepatology, 67(4), 829-846. doi:10.1016/j.jhep.2017.05.016
- Wijarnpreecha K, Thongprayoon C, Ungprasert P (2017). Coffee consumption and risk of nonalcoholic fatty liver disease: a systematic review and meta-analysis. European Journal of Gastroenterology & Hepatology, 29(2), e8-e12. doi:10.1097/MEG.0000000000000776
- Harrison SA et al. (2024). A phase 3, randomized, controlled trial of resmetirom in NASH with liver fibrosis. New England Journal of Medicine, 390(6), 497-509. doi:10.1056/NEJMoa2309000
- Sanyal AJ et al. (2025). Phase 3 trial of semaglutide in metabolic dysfunction-associated steatohepatitis. New England Journal of Medicine, 392(21), 2089-2099. doi:10.1056/NEJMoa2413258
- Sanyal AJ et al. (2010). Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. New England Journal of Medicine, 362(18), 1675-1685. doi:10.1056/NEJMoa0907929
- Wah Kheong C, Nik Mustapha NR, Mahadeva S (2017). A randomized trial of silymarin for the treatment of nonalcoholic steatohepatitis. Clinical Gastroenterology and Hepatology, 15(12), 1940-1949. doi:10.1016/j.cgh.2017.04.016
- Yan HM et al. (2015). Efficacy of berberine in patients with non-alcoholic fatty liver disease. PLoS One, 10(8), e0134172. doi:10.1371/journal.pone.0134172
- Fischer LM et al. (2007). Sex and menopausal status influence human dietary requirements for the nutrient choline. American Journal of Clinical Nutrition, 85(5), 1275-1285. doi:10.1093/ajcn/85.5.1275
- Buchman AL et al. (1995). Choline deficiency: a cause of hepatic steatosis during parenteral nutrition that can be reversed with intravenous choline supplementation. Hepatology, 22(5), 1399-1403. PubMed 7590654
- Commission Regulation (EU) No 432/2012 of 16 May 2012 establishing a list of permitted health claims made on foods, other than those referring to the reduction of disease risk and to children’s development and health. Official Journal of the European Union, L 136, 25.5.2012, p. 1-40. eur-lex.europa.eu
Food supplements are not a substitute for a varied and balanced diet and a healthy lifestyle. Ask a healthcare professional for advice if you are taking medication, are pregnant or are breastfeeding.
