Fatty Liver Disease (MASLD, Formerly NAFLD): What It Means and How Low-Carb Nutrition Can Help

Fatty liver disease is common, often silent and closely connected to insulin resistance. Many people discover it only after an imaging study shows fat in the liver or routine bloodwork shows an elevated liver enzyme. Others have normal liver enzymes despite significant disease.

The encouraging news is that liver fat can change quickly. Improving metabolic health, reducing excess weight when present, exercising and changing the composition of the diet can all help. Carbohydrate restriction—including a well-formulated ketogenic diet—is a legitimate therapeutic option with increasingly strong evidence for people with fatty liver, obesity, prediabetes or type 2 diabetes.

The goal is not merely to lower a liver-enzyme result. It is to reduce liver fat, identify or prevent fibrosis and address the metabolic and cardiovascular risks that commonly travel with fatty liver.

The names have changed: MASLD and MASH

The condition historically called nonalcoholic fatty liver disease (NAFLD) is now called metabolic dysfunction-associated steatotic liver disease (MASLD). The inflammatory form historically called nonalcoholic steatohepatitis (NASH) is now called metabolic dysfunction-associated steatohepatitis (MASH).[1]

These updated names place the emphasis where it belongs: metabolic dysfunction. We will use MASLD and MASH throughout this article while retaining NAFLD and NASH where helpful because patients, clinicians and older studies still use those terms.

The spectrum includes:

• Steatosis: excess fat stored in the liver.
• MASH: liver fat accompanied by inflammation and liver-cell injury.
• Fibrosis: scar tissue that develops as injury persists.
• Cirrhosis: advanced scarring that changes the structure and function of the liver.

MASLD is not the same as alcohol-related liver disease. People with both metabolic dysfunction and more than minimal alcohol exposure may fall into a category called MetALD. Medication-related liver injury, viral hepatitis, autoimmune disease, genetic disorders and other causes of liver disease also require consideration.[1,2]

Why fatty liver matters

Most people with uncomplicated steatosis will not develop liver failure. The clinical priority is identifying the smaller group with significant fibrosis or a higher likelihood of progression.

Advanced fibrosis increases the risk of cirrhosis, liver failure and liver cancer. MASLD also travels with increased risks of type 2 diabetes, cardiovascular disease, chronic kidney disease and other metabolic complications. For many people with MASLD, cardiovascular disease represents a greater near-term threat than liver failure.[2,3,17]

This is why fatty liver should be treated as a whole-body metabolic signal rather than an isolated imaging finding.

What causes fat to accumulate in the liver?

The liver helps regulate glucose, fats and energy storage. Liver fat can accumulate when the delivery and production of fatty acids exceed the liver’s ability to oxidize or export them.

Several processes can contribute:

• Insulin resistance and chronically elevated insulin
• Excess energy intake and expansion of visceral fat
• Release of fatty acids from insulin-resistant adipose tissue
• Hepatic de novo lipogenesis—the creation of new fat from carbohydrate substrates
• High intake of refined carbohydrates and added sugars, particularly fructose-containing sugars
• Genetics, sleep apnea, hormonal conditions, medications and other health factors
• Alcohol exposure, which must be assessed separately even when metabolic risk is also present

Refined carbohydrates and added sugars can be important drivers, but it would be inaccurate to claim that they are the only causes. MASLD develops from an interaction among metabolic health, diet, body-fat distribution, genetics, activity, sleep, alcohol exposure and other clinical factors.

Sugar restriction can reduce liver fat before major weight loss

One of the original Toward Health article’s central studies examined 41 children with obesity and habitual high sugar intake. Researchers provided food for nine days while keeping total energy and overall macronutrient composition similar to the participants’ baseline diets. They replaced much of the dietary sugar with starch.[4]

Median liver fat decreased from 7.2% to 3.8%. Hepatic de novo lipogenesis decreased from 68% to 26%, visceral fat declined and insulin kinetics improved. Because this was a short, uncontrolled before-and-after intervention in a specific pediatric population, it does not establish that all starch is harmless or that calorie balance never matters. It does show that carbohydrate type—and particularly heavy exposure to fructose-containing sugar—can influence liver metabolism beyond a simple calorie count.[4]

What the newest controlled trial found

A randomized clinical trial published online in Cell Metabolism on August 27, 2026 directly tested whether macronutrient composition changes the metabolic response to matched weight loss.[5]

The investigators randomized 55 adults with obesity, prediabetes and hepatic steatosis to one of three fully provided diets:

• A very-low-carbohydrate ketogenic diet
• A Mediterranean diet
• A very-low-fat, plant-forward diet

Forty-two participants completed the study. Each group lost approximately 10% of its starting weight over roughly four to five months, allowing the researchers to examine differences associated with diet composition rather than unequal weight loss.

All three diets improved health. Skeletal-muscle insulin sensitivity increased by approximately 50% in every group without a significant difference among diets. The liver response, however, differed:

• The increase in hepatic insulin sensitivity was two to three times greater in the ketogenic group than in the Mediterranean and very-low-fat groups.
• Intrahepatic triglyceride content decreased by 67% with the ketogenic diet, compared with 45% in each higher-carbohydrate group.
• Hepatic de novo lipogenesis, glycated hemoglobin and 24-hour glucose and insulin exposure decreased most in the ketogenic group.
• Prediabetes remission occurred in 50% of ketogenic participants, 29% of Mediterranean participants and 7% of very-low-fat participants.
• Fasting triglycerides improved more with the ketogenic diet. However, 24-hour triglyceride exposure, LDL cholesterol and apolipoprotein B did not differ among groups.

This is important condition-specific evidence that dietary carbohydrate restriction can improve liver metabolism beyond the benefit of weight loss alone.

The study was also small and relatively short, all meals were supplied, and participants had the specific combination of obesity, prediabetes and hepatic steatosis. It does not establish long-term liver or cardiovascular outcomes, and it does not tell us whether a less restrictive low-carbohydrate diet would produce the same results.[5]

What the broader low-carbohydrate evidence shows

The newest trial builds on several earlier studies:

• In the CENTRAL trial, a low-carbohydrate Mediterranean pattern reduced hepatic fat more than a low-fat diet even after accounting for visceral-fat changes.[6]
• In a small randomized trial of adolescents with obesity and fatty liver, an eight-week moderately carbohydrate-restricted diet improved insulin resistance and body composition more than a fat-restricted diet. Liver fat declined significantly within the carbohydrate-restricted group, although the between-group difference in liver-fat change was not significant.[7]
• In ten adults with overweight or obesity and NAFLD, six days of a ketogenic diet reduced intrahepatic triglyceride content by 31% and hepatic insulin resistance by 58%, alongside approximately 3% weight loss.[8]
• A two-week isocaloric carbohydrate-restricted intervention produced rapid reductions in liver fat and de novo lipogenesis in adults with obesity and NAFLD.[9]
• In older adults with obesity, eight weeks of a very-low-carbohydrate diet produced greater loss of visceral and intermuscular fat and greater improvement in insulin sensitivity than a low-fat diet. This trial was not specifically a fatty-liver treatment study, but it supports the broader metabolic rationale.[10]
• A randomized controlled feeding trial found that fructose- and sucrose-sweetened beverages, but not glucose-sweetened beverages, increased hepatic de novo lipogenesis.[11]
• A prospective eight-week study of 33 adults with overweight or obesity found reductions in weight, insulin resistance, liver enzymes and the FibroScan controlled attenuation parameter during a very-low-calorie ketogenic program. Its uncontrolled design limits causal conclusions.[12]

Taken together, the evidence supports carbohydrate restriction as an effective option for reducing liver fat and improving insulin resistance. The size of the effect, the need for weight loss and the most sustainable level of carbohydrate restriction will differ among individuals.

Federal guidance now recognizes carbohydrate restriction

The Dietary Guidelines for Americans, 2025–2030 states that people with certain chronic diseases may experience improved outcomes with a lower-carbohydrate diet and should work with a healthcare professional to identify an approach appropriate for their condition.[13]

The accompanying scientific appendix explicitly defines a ketogenic diet as a carbohydrate-restricted dietary pattern, generally providing 20–50 grams of carbohydrate per day or less than 10% of energy from carbohydrate.[14]

This places carbohydrate restriction and ketogenic nutrition within the recognized scientific framework for chronic-disease nutrition. It supports considering these approaches across chronic-disease care when the evidence and clinical circumstances fit rather than dismissing them categorically. In MASLD, the recent controlled evidence provides a direct clinical reason to consider them.

How fatty liver is evaluated

Fatty liver is often first suspected because of:

• Fat seen on ultrasound, CT or MRI
• Elevated ALT or AST
• Type 2 diabetes, prediabetes or metabolic syndrome
• Abdominal obesity, high triglycerides or other cardiometabolic risks

Normal ALT and AST do not rule out MASH or advanced fibrosis. Routine ultrasound can detect moderate or severe steatosis but may miss lesser degrees, particularly in people with obesity. MRI-based methods can quantify liver fat more accurately, although they are not necessary for every patient.[2,3]

Fibrosis risk matters more than the amount of fat alone

The most important clinical question is often not simply “Is fat present?” but “Is significant scarring present?”

Guidelines recommend a stepwise noninvasive assessment for people with steatosis or relevant metabolic risk. The FIB-4 score, calculated from age, AST, ALT and platelet count, is commonly used as a first assessment. A low score can help rule out advanced fibrosis in many adults. An elevated or indeterminate result may lead to vibration-controlled transient elastography, the Enhanced Liver Fibrosis test, magnetic resonance elastography or hepatology referral.[2,3]

FIB-4 has important age-related limitations and should not be interpreted in isolation during acute illness. Thresholds and reassessment intervals depend on age, diabetes status, the clinical setting and the guideline being followed. A clinician should interpret the result rather than treating an online calculator as a diagnosis.[2]

A liver biopsy is no longer required for every patient. It is generally reserved for selected situations involving diagnostic uncertainty, conflicting noninvasive results or a need to establish the type and stage of liver injury.[2]

Treatment: address the liver and the whole metabolic picture

Reduce refined carbohydrates and added sugars

Removing sugar-sweetened beverages and substantially reducing refined carbohydrates can directly reduce substrates and hormonal signals that promote hepatic fat production. The improvement seen during fructose restriction can occur before major weight loss.[4,11]

Consider therapeutic carbohydrate restriction

A low-carbohydrate or ketogenic plan can reduce liver fat, insulin levels, glucose exposure, appetite and other metabolic risks. A practical whole-food plan generally emphasizes adequate protein, minimally processed foods, nonstarchy vegetables as tolerated and fats appropriate to the person’s energy needs and cardiometabolic profile.

The plan should be designed around medical history, medications, nutrient needs, food preferences and the ability to sustain it. People using insulin, sulfonylureas, SGLT2 inhibitors, blood-pressure medication or other therapies that may require adjustment should make major dietary changes with clinical supervision.

Pursue meaningful weight loss when excess weight is present

Weight loss remains a powerful treatment. AASLD guidance notes that modest weight loss can improve steatosis, while greater and sustained loss is generally needed to improve MASH and fibrosis.[2] The right target is individual; the new Cell Metabolism trial shows that diet composition may add benefits even when weight loss is matched.[5]

Exercise even when weight loss is limited

Both aerobic and resistance exercise can improve insulin sensitivity, cardiometabolic fitness and liver health. Exercise can reduce liver fat even when the scale changes little. The safest and most useful program is one the person can perform consistently.

Address alcohol and associated conditions

Alcohol exposure should be assessed honestly because it can worsen liver injury and alter the diagnosis. Treatment should also address type 2 diabetes, sleep apnea, hypertension, dyslipidemia and other cardiovascular risks.

Medication is available for selected people with MASH and fibrosis

Lifestyle and metabolic treatment remain foundational, but medication options have expanded. The FDA approved resmetirom in 2024, with diet and exercise, for adults with noncirrhotic MASH/NASH and moderate-to-advanced fibrosis.[15] In 2025, the FDA approved semaglutide for adults with noncirrhotic MASH and moderate-to-advanced fibrosis.[16]

These are not medications for every person with simple steatosis. Their potential benefits, contraindications, adverse effects, monitoring requirements and cost require an individualized discussion. Suspected advanced fibrosis or cirrhosis warrants specialist involvement.

When to seek medical attention

Fatty liver is usually not an emergency, but jaundice, increasing abdominal swelling, vomiting blood, black stools, new confusion, marked weakness or severe persistent abdominal pain requires prompt medical evaluation.

People with persistently abnormal liver tests, signs of advanced fibrosis, unexplained liver disease or conflicting test results should be evaluated for other causes and referred when appropriate.

The takeaway

Fatty liver is a metabolic warning sign, but it is not a fixed destiny. The liver can respond rapidly to changes in sugar exposure, carbohydrate intake, insulin levels, activity and body weight.

Recent controlled evidence strengthens the case for therapeutic carbohydrate restriction. With matched weight loss, a very-low-carbohydrate ketogenic diet produced greater improvements in hepatic insulin sensitivity and liver fat than Mediterranean and very-low-fat diets in adults with obesity, prediabetes and hepatic steatosis.[5]

The best plan combines an effective dietary strategy with appropriate fibrosis assessment, exercise, management of associated conditions and medication when indicated. Progress should be judged by the whole clinical picture—not one liver enzyme, one scan or one number on the scale.

References

1. Rinella ME, Lazarus JV, Ratziu V, et al. A multisociety Delphi consensus statement on new fatty liver disease nomenclature. J Hepatol. 2023;79(6):1542–1556. doi: 10.1016/j.jhep.2023.06.003

2. Rinella ME, Neuschwander-Tetri BA, Siddiqui MS, et al. AASLD Practice Guidance on the clinical assessment and management of nonalcoholic fatty liver disease. Hepatology. 2023;77(5):1797–1835. doi: 10.1097/HEP.0000000000000323

3. European Association for the Study of the Liver; European Association for the Study of Diabetes; European Association for the Study of Obesity. EASL-EASD-EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD). J Hepatol. 2024. PubMed Central

4. Schwarz JM, Noworolski SM, Erkin-Cakmak A, et al. Effects of Dietary Fructose Restriction on Liver Fat, De Novo Lipogenesis, and Insulin Kinetics in Children With Obesity. Gastroenterology. 2017;153(3):743–752. doi: 10.1053/j.gastro.2017.05.043. PubMed

5. Petersen MC, Smith GI, Farabi SS, Palacios HH, Shankaran M, Hellerstein MK, Patterson BW, Klein S. Effect of diet macronutrient content on the cardiometabolic response to weight loss: A randomized clinical trial. Cell Metab. Published online August 27, 2026. doi: 10.1016/j.cmet.2026.07.020

6. Gepner Y, Shelef I, Komy O, et al. The beneficial effects of Mediterranean diet over low-fat diet may be mediated by decreasing hepatic fat content. J Hepatol. 2019;71(2):379–388. PubMed

7. Goss AM, Dowla S, Pendergrass M, et al. Effects of a carbohydrate-restricted diet on hepatic lipid content in adolescents with non-alcoholic fatty liver disease: a pilot, randomized trial. Pediatr Obes. 2020;15(7):e12630. doi: 10.1111/ijpo.12630. PubMed

8. Luukkonen PK, Dufour S, Lyu K, et al. Effect of a ketogenic diet on hepatic steatosis and hepatic mitochondrial metabolism in nonalcoholic fatty liver disease. Proc Natl Acad Sci U S A. 2020;117(13):7347–7354. PubMed. Original article link

9. Mardinoglu A, Wu H, Bjornson E, et al. An Integrated Understanding of the Rapid Metabolic Benefits of a Carbohydrate-Restricted Diet on Hepatic Steatosis in Humans. Cell Metab. 2018;27(3):559–571.e5. doi: 10.1016/j.cmet.2018.01.005. PubMed

10. Goss AM, Gower B, Soleymani T, et al. Effects of weight loss during a very low carbohydrate diet on specific adipose tissue depots and insulin sensitivity in older adults with obesity: a randomized clinical trial. Nutr Metab (Lond). 2020;17:64. doi: 10.1186/s12986-020-00481-9. Original full text

11. Geidl-Flueck B, Hochuli M, Németh Á, et al. Fructose- and sucrose- but not glucose-sweetened beverages promote hepatic de novo lipogenesis: A randomized controlled trial. J Hepatol. 2021. PubMed

12. Rinaldi R, De Nucci S, Castellana F, et al. The Effects of Eight Weeks’ Very Low-Calorie Ketogenic Diet (VLCKD) on Liver Health in Subjects Affected by Overweight and Obesity. Nutrients. 2023;15(4):825. doi: 10.3390/nu15040825. PubMed

13. U.S. Department of Health and Human Services and U.S. Department of Agriculture. Dietary Guidelines for Americans, 2025–2030. 10th ed. January 2026. Official PDF

14. U.S. Department of Health and Human Services and U.S. Department of Agriculture. The Scientific Foundation for the Dietary Guidelines for Americans, 2025–2030: Appendices. Definition of carbohydrate-restricted and ketogenic dietary patterns. Official PDF

15. U.S. Food and Drug Administration. FDA Approves First Treatment for Patients with Liver Scarring Due to Fatty Liver Disease. March 14, 2024. FDA

16. U.S. Food and Drug Administration. FDA Approves Treatment for Serious Liver Disease Known as MASH. August 15, 2025. FDA

17. Rana H, Yip TCF, Lim BL, et al. Non-alcoholic Fatty Liver Disease: Growing Burden, Adverse Outcomes and Associations. J Clin Transl Hepatol. 2020. PubMed