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Fatty Liver · MASLD (formerly NAFLD)
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In one pass Fatty liver means liver cells packed with fat droplets they were never meant to hold, so that the liver is being used as a fat store.
Educational content, not medical advice — consult a clinician.
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Chapter 1
What fatty liver is, and its new name
Fatty liver means liver cells packed with fat droplets they were never meant to hold, so that the liver is being used as a fat store. It used to be thought of mainly as a drinking problem; for most people the real driver is metabolic dysfunction, the same cluster as high blood glucose, a large waist and disordered blood lipids. In 2023 a consensus of several international liver societies renamed it metabolic dysfunction-associated steatotic liver disease, or (formerly NAFLD), because the old name only said what it is not: caused by alcohol.
At first it causes no symptoms. Left for years, the liver can become inflamed and scarred, but what usually kills first is heart and blood-vessel disease, not the liver itself: the same metabolic disorder harms both. Yellowing of the skin or the whites of the eyes, vomiting blood or passing black stools, a markedly swollen belly, or confusion are signs of decompensated cirrhosis — seek medical care immediately.
At first it causes no symptoms. Left for years, the liver can become inflamed and scarred, but what usually kills first is heart and blood-vessel disease, not the liver itself: the same metabolic disorder harms both. Yellowing of the skin or the whites of the eyes, vomiting blood or passing black stools, a markedly swollen belly, or confusion are signs of decompensated cirrhosis — seek medical care immediately.
Clinical · How to tell whether the liver is scarred
The most common misunderstanding about fatty liver is this: an ultrasound report that says "fatty liver" does not tell you how far the disease has gone. What decides the outlook is not whether fat is present but whether there is fibrosis (scar tissue growing in the liver), so the real focus of diagnosis is staging.Step one is finding the fat. A routine abdominal ultrasound picks up moderate to severe fatty liver but is insensitive to mild fat (< 20%). The liver enzyme can be entirely normal, so "normal liver function" does not rule out . More sensitive tools are the controlled attenuation parameter (CAP) measured by FibroScan, and MRI-PDFF on magnetic resonance imaging, both of which put a number on the share of fat in the liver.
Step two is the decisive one: assessing fibrosis. The most practical tools are a few non-invasive scores:
The FIB-4 index: calculated from age, ALT, and platelet count — four routine results — so it is free and available any time. FIB-4 < 1.3 largely rules out advanced fibrosis; > 2.67 calls for further assessment.The NFS fibrosis score (its name still uses the old term): a similar idea, adding body mass index () and blood glucose.FibroScan elastography (liver stiffness measurement, LSM): transient elastography measures how stiff the liver is, which is more direct than a score.
Liver biopsy is still the gold standard, but it is invasive and subject to sampling error; it is now used mainly when non-invasive assessment is inconclusive or for entry into clinical trials.
A reasonable order in practice: screen first with a free score such as FIB-4. People with a low score need only periodic follow-up; those with an intermediate or high score, or with a high-risk background such as diabetes, go on to FibroScan or a referral to a liver specialist. That puts limited testing where it is actually needed.
Numbers · Diagnostic criteria, stages, how common
Diagnosis rests on two things (the 2023 definition, Rinella 2023): first, imaging or biopsy showing fat in ≥ 5% of liver cells; second, at least 1 of 5 cardiometabolic risk factors — overweight or obesity (body mass index, , ≥ 25, or ≥ 23 in people of Asian ancestry), fasting glucose ≥ 5.6 mmol/L or (HbA1c) ≥ 5.7%, blood pressure ≥ 130/85 mmHg, (TG) ≥ 1.7 mmol/L, or high-density lipoprotein cholesterol () ≤ 1.0 mmol/L in men or ≤ 1.3 mmol/L in women (taking a drug for the condition also counts).The disease is divided into stages by severity: the mildest is simple steatosis, with fat deposits but no inflammation. Next is metabolic dysfunction-associated steatohepatitis (MASH, formerly NASH): fat plus inflammation plus ballooning of liver cells (injured cells that swell and round up), which is the type that can progress. Further on, fibrosis is graded from F0 to F4, and the risk of cirrhosis and liver cancer rises clearly from F3 up. The end point is decompensated cirrhosis, at which stage a liver transplant has to be considered. Most people stay at simple steatosis for the long term; what decides the outcome is whether scarring develops. Still, it is not harmless: an often-quoted estimate is that 10–25% of people with MASH progress to cirrhosis within 10 years.
It is anything but rare: about 25% of adults worldwide have fatty liver (Younossi 2018), and a pooled estimate for China is about 29.2% (Zhou 2019). Both studies used the old definition from before the rename, and the figures rise with obesity rates. Among people with type 2 diabetes, common estimates are that 55–75% also have fatty liver, rising to 75% among people with obesity (BMI ≥ 30).
There is still no dedicated drug for the whole course of the disease: resmetirom is the first drug approved by the US FDA for MASH, but only for stages F2–F3, and it must be combined with lifestyle change, not used instead of it.
Chapter 2
Why fat builds up in the liver
Fat usually gets into the liver because of insulin resistance. Fat tissue stops storing fat properly, so large amounts of free fatty acids flood into the liver; at the same time, a diet high in sugar, especially fructose, forces the liver to turn sugar into fat itself. More comes in than is shipped out, and fat droplets keep piling up inside liver cells.
The stored fat is itself toxic: it wears down the mitochondria and sets off inflammation. Liver cells are injured and die, and meanwhile another type of cell is stimulated to secrete collagen to patch the damage, so simple steatosis moves on to hepatitis and then to fibrosis. The same metabolic disorder is also harming the blood vessels; the liver is often just the first warning light to come on. Whether someone stays stable for decades or progresses within a few years depends on their genes, their metabolic background and how they live.
The stored fat is itself toxic: it wears down the mitochondria and sets off inflammation. Liver cells are injured and die, and meanwhile another type of cell is stimulated to secrete collagen to patch the damage, so simple steatosis moves on to hepatitis and then to fibrosis. The same metabolic disorder is also harming the blood vessels; the liver is often just the first warning light to come on. Whether someone stays stable for decades or progresses within a few years depends on their genes, their metabolic background and how they live.
Mechanism · Why sugary drinks hit the liver hardest
Of the routes by which fat gets into the liver, one deserves its own page: de novo lipogenesis (DNL, the liver building fat directly from sugar). It is the core mechanism by which sugary drinks and juice harm the liver, and the reason cutting sugar pays off most in fatty liver. A common estimate is that in this pathway can run at 3–5 times its usual rate. On top of that, the liver cannot ship out in very-low-density lipoprotein (VLDL) as fast as it is coming in, so fat keeps piling up inside liver cells.Glucose can be used by cells all over the body, and once insulin gives the signal, muscle and fat tissue share the load. Fructose is different: it is metabolized mainly in the liver, its first steps are not regulated by insulin, and it has no rate-limiting checkpoint of the kind glucose has. So the fructose in one large sugary drink lands, concentrated, on a single organ, the liver (Tappy 2010 review).
The liver cannot burn all that fructose in time, so it routes it through DNL into fatty acids and then triglycerides. In Stanhope 2009's controlled trial, adults with overweight or obesity drank sweetened beverages supplying 25% of their daily energy needs for 10 weeks. Both groups gained about the same weight, but only the fructose group showed a clear rise in visceral fat, higher DNL in the liver, worse after-meal blood fats and markers such as low-density lipoprotein, and lower insulin sensitivity; the group drinking the same amount of glucose did not respond the same way. Same calories, completely different metabolic fate. The dose in this trial was large, and liver fat was not measured directly. A 2012 commentary in Nature by Lustig and colleagues summed it up: not all sugar is the same, and fructose's burden on the liver is unusually concentrated.
That is why cutting sugary drinks and juice comes first in dietary treatment for MASLD. Note that this means added sugar and concentrated juice — large doses that reach the liver fast. Whole fruit contains less fructose, wrapped in fiber and absorbed far more slowly; it is not in the same league, and there is no need to fear fruit.
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Mechanism · From fat to inflammation, scar and heart
The second step is when this stored fat starts causing harm. The fat is itself toxic: lipids such as saturated fats, ceramides and diacylglycerols (DAGs) switch on inflammatory pathways, the mitochondria are worn down and oxidative stress rises. When the gut barrier loosens, fragments of bacterial walls — lipopolysaccharide (LPS) — leak into the blood and activate the liver's resident immune cells (Kupffer cells), and inflammation takes hold. Liver cells are injured and die, and hepatic stellate cells are activated to secrete collagen to patch the damage, so simple steatosis moves on to steatohepatitis (MASH) and then to fibrosis.Why do some people stay stable for decades while others progress within a few years? It comes down to a few things: genes (for example a variant of the PNPLA3 gene, whose carriers build up liver fat more readily), metabolic background (people who also have diabetes, high blood lipids or high blood pressure progress faster), lifestyle (alcohol, sitting, ultra-processed food and high fructose all speed it up), and where fat sits in the body.
Do not forget the heart: the same metabolic disorder harms both the liver and the blood vessels. An often-quoted estimate is that heart and blood-vessel disease is about 2 times as common in people with fatty liver as in others; this is an observed association, with the same cluster of metabolic problems behind both. The liver is often just the first warning light, so a diagnosis of fatty liver is also notice to assess and manage cardiovascular risk at the same time.
Clinical · Can you have fatty liver without being heavy?
Many people assume fatty liver is a problem only for heavier people, but lean fatty liver (lean ) is real: with a body mass index () under 25 (under 23 for people of Asian ancestry), a person can still have it if visceral fat is high and muscle is low. This explains two things: why some very lean people are found to have fatty liver, and why the same fatty liver leaves some people fine for decades while others move quickly to cirrhosis.What usually lies behind lean fatty liver is where fat is stored, not total body weight. People whose fat under the skin can "hold" only a limited amount are more likely to pile the excess into the organs and the liver (ectopic fat). At the same time, low muscle mass (sarcopenia) leaves glucose fewer places to go and worsens insulin resistance. So someone who does not look heavy but has a large waist, little muscle, a sugary-drink habit and a sedentary life can still have fatty liver.
Genes are an easily underestimated factor too. The I148M variant of the PNPLA3 gene is one of the known genetic variants with the largest effect on liver fat; carriers build up liver fat more readily on the same diet and progress more easily. This is not fate: genes set the starting line, but diet, exercise, sugary drinks and alcohol still drive the finish. People who carry a high-risk variant are, if anything, the ones for whom solid lifestyle habits matter most.
Whatever your weight, the outcome is decided by fibrosis. Kim 2013 analyzed about 11,000 adults in a US national health survey (using the old definition from before the rename), followed for a median of 14.5 years. Fatty liver found on ultrasound did not, by itself, raise the death rate; but the group whose non-invasive scores pointed to advanced fibrosis had about a 69% higher risk of death, almost all of it from cardiovascular causes. This was an observational study.
What it means in practice: if a check-up finds fatty liver, do not dismiss it because "I'm not heavy". The fibrosis assessment, cardiovascular risk and blood glucose and lipid checks all still apply.
Chapter 3
Liver scarring and current drugs
The truly dangerous turning point in fatty liver is not how much fat has built up but whether scarring has begun. For most people, simple steatosis stays stable for the long term. What decides the outcome of the liver disease is how far fibrosis has gone, which predicts the future better than liver enzymes or the amount of fat.
Scar forms like this: liver cells are injured again and again by fat toxicity and inflammation, and hepatic stellate cells are activated, turn into myofibroblasts and pour out collagen. Early fibrosis can recede once its drivers are removed (weight loss, metabolic control); after the structural changes of cirrhosis, it mostly cannot. The drugs that exist are all add-ons to this main line.
Scar forms like this: liver cells are injured again and again by fat toxicity and inflammation, and hepatic stellate cells are activated, turn into myofibroblasts and pour out collagen. Early fibrosis can recede once its drivers are removed (weight loss, metabolic control); after the structural changes of cirrhosis, it mostly cannot. The drugs that exist are all add-ons to this main line.
Mechanism · Why the fibrosis stage matters most
Seeing this path clearly explains why doctors watch the stage, not just whether fat is present. Simple steatosis stays stable for the long term in most people; the truly dangerous turn is progression to metabolic dysfunction-associated steatohepatitis (MASH: fat plus inflammation plus ballooning of liver cells), and on to fibrosis.Fibrosis stage is the single strongest predictor of long-term outcome, stronger than and stronger than the amount of fat. F0–F2 carries lower risk; F3 (bridging fibrosis, where scars have joined up into bridges) and F4 (cirrhosis) are the main sources of cirrhosis complications, liver cancer, liver failure and death from liver disease.
Scar forms like this: liver cells are injured again and again by fat toxicity and inflammation, and hepatic stellate cells (HSCs) are activated, turn into myofibroblasts and secrete large amounts of collagen. Early fibrosis is reversible once the drivers are removed (weight loss, metabolic control); after the structural changes of cirrhosis it is largely irreversible.
Vilar-Gomez 2015, a prospective cohort study (not a randomized trial), observed exactly this. At a hospital in Cuba, 293 patients with biopsy-proven steatohepatitis (then called NASH, now MASH) were encouraged to change their lifestyle and lose weight over a year, with a liver biopsy at the start and at week 52. The more weight people lost, the more every histological feature of steatohepatitis improved; among those who lost ≥ 10% of their weight, fibrosis receded in 45%. Take the driver away, and early scarring has a chance to recede.
Clinical · What the current drugs can do
For decades had no approved drug of its own, because its driver is whole-body metabolism and a single target rarely moves it. Even now that a drug exists, weight loss and metabolic management are still the foundation; drugs are add-ons, not a shortcut around lifestyle.In 2024, resmetirom (brand name Rezdiffra) became the first drug approved by the US FDA specifically for MASH. It is a thyroid hormone receptor-β (THR-β) agonist that increases fat burning in the liver. It is used only for stages F2–F3, and it must be added on top of lifestyle change, not used instead of it.
Glucagon-like peptide-1 () receptor agonists (semaglutide, tirzepatide) were developed to lower blood glucose and body weight, but their strong weight loss brings improvement in MASH histology, and that improvement has been seen in trials; they fit especially well for people who also have obesity or type 2 diabetes. Vitamin E at 800 a day is an option for people with MASH who do not have diabetes (based on the PIVENS ), but high doses over the long term raise cardiovascular concerns, so it is not for everyone. Pioglitazone improves MASH histology but causes weight gain and raises the risk of heart failure, so it is used selectively. All of these are decisions for a doctor to make after assessment.
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Chapter 4
Treatment · 7-10% weight loss
The lever that really moves is weight and metabolism, not a pill. The fat droplets in liver cells follow the whole body's energy ledger: take in a little less, burn a little more, and liver cells get a chance to clear out the fat they have stored.
Vilar-Gomez 2015 was a prospective cohort study, not a randomized trial: 293 patients with biopsy-proven steatohepatitis lost weight through lifestyle change over a year, and the more they lost, the more their liver histology improved. Among those who lost ≥ 10% of their weight, steatohepatitis resolved in 90%. On this basis the American Association for the Study of Liver Diseases (AASLD) 2018 guidance treats 7–10% as the target for improving inflammation and scarring. Drugs can be added, but they cannot replace this main line.
Vilar-Gomez 2015 was a prospective cohort study, not a randomized trial: 293 patients with biopsy-proven steatohepatitis lost weight through lifestyle change over a year, and the more they lost, the more their liver histology improved. Among those who lost ≥ 10% of their weight, steatohepatitis resolved in 90%. On this basis the American Association for the Study of Liver Diseases (AASLD) 2018 guidance treats 7–10% as the target for improving inflammation and scarring. Drugs can be added, but they cannot replace this main line.
Numbers · How much weight loss changes what
Weight loss is not a "the more the better" slogan; it is a dose-response in which each step lines up with a change in liver tissue.The AASLD 2018 guidance (Chalasani 2018) puts it this way: losing at least 3–5% of body weight is needed to improve steatosis, and improving most histological features of steatohepatitis, fibrosis included, takes 7–10%. An often-quoted estimate is that a 3–5% loss lowers liver fat by roughly 30–50%.
The Vilar-Gomez 2015 cohort gives finer figures (a prospective cohort of 293 patients, one year, liver biopsies before and after):
Among the 88 people who lost ≥ 5%, steatohepatitis resolved in 58% and the disease activity score fell by at least 2 points in 82%; those who lost less did clearly worse.Everyone who lost 7–10% and had few risk factors saw their activity score fall.Everyone who lost ≥ 10% saw their activity score fall; steatohepatitis resolved in 90% and fibrosis receded in 45%.But only about three in ten people lost more than 5% within the year: the hard part is actually doing it.
That is why 7–10% is so often written as the core target: the first kilograms mainly clear fat droplets from the liver, and only further down do inflammation and scarring start to move. Falling short of 10% is not wasted effort, since 3–5% already moves liver fat. Drugs can sit on top of this curve; they cannot replace it with a pill.
In practice · What to eat, how to move, and alcohol
Diet: current guidelines put a Mediterranean eating pattern first — rich in monounsaturated fat and polyphenols, with fish, vegetables, fruit and whole grains. Limiting sugar and fructose ranks near the top: sugary soft drinks and juice are the leading burden on the liver, and giving them up pays off most. Ultra-processed food brings high fat, high sugar and additives all at once and is worth cutting down. There is no need for extreme low-fat or low-carbohydrate diets; the emphasis is on quality, not ratios.Exercise: exercise helps liver fat even when body weight barely changes. With 150–200 minutes of aerobic exercise a week, liver fat falls; strength training improves insulin sensitivity and keeps muscle. Aerobic plus strength training works better than either alone.
Alcohol: for the liver, the less the better. The often-quoted "under 30 g a day for men and under 20 g for women" is really a classification line, not a safe amount: under the 2023 nomenclature (Rinella 2023), a woman drinking more than 140 g of alcohol a week, or a man more than 210 g, no longer has plain but metabolic dysfunction and alcohol-related liver disease (MetALD). People who already have MASH with fibrosis at F2 or beyond are usually advised to stop drinking completely — alcohol and MASH together speed up fibrosis.
Clinical · Drugs as add-ons, and how often to recheck
Vitamin E, pioglitazone, drugs and resmetirom are all add-ons, layered on top of the main line of weight loss and metabolic management (who each one suits is covered in the chapter Liver scarring and current drugs). Approaches such as time-restricted eating still have limited clinical evidence and are not strongly recommended here.How often to recheck: assess fibrosis at diagnosis (FIB-4, the NFS score, FibroScan); after that, people at low risk recheck liver tests, FIB-4, and metabolic and cardiovascular markers every 1–3 years. Anyone with fibrosis at F3 or beyond is referred to a liver specialist and screened for liver cancer (an abdominal ultrasound every 6 months).
Chapter 5
I have fatty liver — what now?
If a check-up says fatty liver, do not fix on the ultrasound wording alone. Two things come first: how far scarring in the liver has gone, and the body's metabolic background — blood glucose, blood lipids, blood pressure, waist size — because the same disorder harms both the liver and the blood vessels.
The strongest lever is usually not a drug but weight loss, cutting out sugary drinks, and then adding exercise. Fatty liver almost never comes alone; it is metabolic syndrome showing up in the liver. Most people at an early stage should get the lifestyle work solid first; drugs come into the conversation with a doctor only when there is fibrosis or another metabolic disease alongside.
The strongest lever is usually not a drug but weight loss, cutting out sugary drinks, and then adding exercise. Fatty liver almost never comes alone; it is metabolic syndrome showing up in the liver. Most people at an early stage should get the lifestyle work solid first; drugs come into the conversation with a doctor only when there is fibrosis or another metabolic disease alongside.
Clinical · Start with a FIB-4
Do not draw conclusions from the ultrasound phrase "fatty liver" alone, and do not assume everything is fine because is normal. First work out a FIB-4 (calculated from age, ALT, and platelet count — free and easy to get).FIB-4 below 1.3: advanced fibrosis is unlikely, so the focus is lifestyle plus regular follow-up. FIB-4 of 1.3 or above, or a high-risk background such as diabetes: go on to FibroScan or a referral to a liver specialist.
Ultrasound answers whether there is fat. FIB-4 and elastography answer whether there is scar. They are not the same diagnosis.
In practice · What to check, and what to do first
Fatty liver almost never comes alone; it is metabolic syndrome showing up in the liver. Check fasting glucose or (HbA1c), blood lipids, blood pressure and waist size at the same time. Cardiovascular disease, not liver disease, is the leading cause of death in people with fatty liver, so a cardiovascular risk assessment must not be skipped.The strongest levers available:
Losing 7–10% of body weight carries the most weight: 3–5% starts to lower liver fat, around 7% starts to improve inflammation, and 10% or more lets fibrosis recede in some people.Cut out sugary drinks and juice: this removes the main raw material for de novo lipogenesis (the liver turning sugar into fat) and pays off fastest.Aerobic exercise plus strength training: liver fat falls even when weight barely moves.Drink less alcohol: fatty liver and alcohol damage the liver together, and people with fibrosis at F2 or beyond are usually advised to stop completely.
Clinical · Whether to take drugs, and when to seek care
Most people at an early stage: do the lifestyle work solidly for 3–6 months, then reassess. With obesity or type 2 diabetes as well: drugs treat the metabolic problem and may also improve the liver, so they are worth discussing with a doctor. MASH at stage F2–F3: resmetirom is a new option, still layered on top of lifestyle change. No drug is a shortcut that replaces weight loss.People at low risk recheck liver tests, FIB-4, and metabolic and cardiovascular markers every 1–3 years. At F3 or beyond: referral to a liver specialist, plus liver-cancer screening (an abdominal ultrasound every 6 months).
Seek medical care immediately for yellowing of the skin or the whites of the eyes (jaundice), a markedly swollen belly (ascites), vomiting blood or black stools (gastrointestinal bleeding), or confusion and drowsiness (hepatic encephalopathy). These are signs of decompensated cirrhosis, not something to keep watching.
In its early and middle stages, fatty liver is a metabolic state that can be treated and is often reversible, not a sentence. It is more like an early metabolic warning slip from your body: read it, follow the main line of weight loss and metabolic health, and most people can bring down their long-term risk to the liver and the heart together.
References · 6
- Rinella, M. E., Lazarus, J. V., Ratziu, V., Francque, S. M., Sanyal, A. J., Kanwal, F., et al. (2023). A multi-society Delphi consensus statement on new fatty liver disease nomenclature. Hepatology, 78(6), 1966-1986. Renames NAFLD to MASLD (metabolic dysfunction-associated steatotic liver disease). Modified Delphi process, 236 panelists from 56 countries, consensus defined as a 67% supermajority. MASLD requires steatosis plus at least 1 of 5 cardiometabolic risk factors; no metabolic parameter and no known cause is cryptogenic steatotic liver disease. MetALD is MASLD with greater alcohol intake: 140-350 g/week for women and 210-420 g/week for men (abstract, PMID 37363821; full text, PMC10653297). 10.1097/HEP.0000000000000520
- Younossi, Z. M., et al. (2018). Global perspectives on nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. Hepatology, 69(6), 2672–2682. 10.1002/hep.30251
- Zhou, F., Zhou, J., Wang, W., Zhang, X. J., Ji, Y. X., Zhang, P., She, Z. G., Zhu, L., Cai, J., & Li, H. (2019). Unexpected rapid increase in the burden of NAFLD in China from 2008 to 2018: a systematic review and meta-analysis. Hepatology, 70(4), 1119-1133. 10.1002/hep.30702
- Chalasani, N., Younossi, Z., Lavine, J. E., Charlton, M., Cusi, K., Rinella, M., et al. (2018). The diagnosis and management of nonalcoholic fatty liver disease: practice guidance from the American Association for the Study of Liver Diseases. Hepatology, 67(1), 328-357. 10.1002/hep.29367
- Kim, D., Kim, W. R., Kim, H. J., & Therneau, T. M. (2013). Association between noninvasive fibrosis markers and mortality among adults with nonalcoholic fatty liver disease in the United States. Hepatology, 57(4), 1357-1365. Design: NHANES III (1988-1994) linked to mortality through 2006 - a US population cohort, not a review. 11,154 participants; ultrasound NAFLD in 34.0%. After a median 14.5 years, ultrasound NAFLD itself was not associated with higher mortality (age- and sex-adjusted HR 1.05, 0.93-1.19). A high probability of advanced fibrosis on noninvasive scores was: NFS HR 1.69 (1.09-2.63), APRI 1.85 (1.02-3.37), FIB-4 1.66 (0.98-2.82), almost entirely from cardiovascular causes. Despite the id, the abstract does not compare lean with obese NAFLD (abstract, PMID 23175136). 10.1002/hep.26156
- Vilar-Gomez, E., Martinez-Perez, Y., Calzadilla-Bertot, L., Torres-Gonzalez, A., Gra-Oramas, B., Gonzalez-Fabian, L., et al. (2015). Weight loss through lifestyle modification significantly reduces features of nonalcoholic steatohepatitis. Gastroenterology, 149(2), 367-378. Prospective single-centre study (Havana), not randomized: 293 patients with biopsy-proven NASH, 52 weeks of lifestyle change, paired biopsies in 261. Overall 25% had NASH resolution and 19% fibrosis regression; 30% lost ≥ 5% of weight. Of those losing ≥ 5%, 58% had NASH resolution. ALL patients losing ≥ 10% had a lower NAFLD activity score, 90% had NASH resolution and 45% had fibrosis regression (abstract, PMID 25865049). 10.1053/j.gastro.2015.04.005