Fatty Liver Disease (MASLD): Symptoms, Diagnosis & NHS Treatment

Metabolic dysfunction-associated steatotic liver disease (MASLD) — formerly known as non-alcoholic fatty liver disease (NAFLD) — is the most common liver condition in the UK, affecting an estimated 1 in 3 adults. It is caused by the accumulation of fat in liver cells in people who drink little or no alcohol, driven by metabolic risk factors including obesity, type 2 diabetes, and high cholesterol. Most people have the simple form (steatosis), but in some, the disease progresses to steatohepatitis, fibrosis, cirrhosis, and liver failure. Lifestyle change remains the cornerstone of treatment, with new drug therapies emerging.

What Is MASLD?

MASLD is defined as the presence of hepatic steatosis (liver fat ≥5%) in the absence of significant alcohol consumption and other secondary causes of liver fat accumulation (viral hepatitis B or C, autoimmune hepatitis, drug-induced liver disease, Wilson’s disease). The updated nomenclature (MASLD, replacing NAFLD) adopted in 2023 reflects the metabolic pathogenesis and carries less stigma than “non-alcoholic” terminology.

The spectrum of MASLD ranges from simple steatosis (fat accumulation without significant inflammation — “MASL”), which is generally benign and reversible, to metabolic dysfunction-associated steatohepatitis (MASH — formerly NASH), which involves hepatocellular inflammation, ballooning degeneration, and necrosis alongside steatosis. MASH drives progressive fibrosis, which can advance to cirrhosis and end-stage liver disease. Hepatocellular carcinoma (HCC) can develop in MASLD-related cirrhosis — and occasionally in advanced fibrosis without cirrhosis.

Risk Factors and Pathophysiology

MASLD is the hepatic manifestation of the metabolic syndrome. Key risk factors include: obesity (BMI above 30, particularly central obesity — approximately 70–90% of people with MASLD have obesity or overweight); type 2 diabetes (present in approximately 50% of people with MASLD, and conferring higher risk of MASH and fibrosis); dyslipidaemia (high triglycerides, low HDL cholesterol); hypertension; insulin resistance; and polycystic ovary syndrome (PCOS). Genetic factors — particularly variants in PNPLA3, TM6SF2, and MBOAT7 genes — significantly modify disease severity and progression risk.

Symptoms of MASLD

The vast majority of people with MASLD — even those with MASH and early fibrosis — have no symptoms. Simple MASLD is almost universally asymptomatic and discovered incidentally through abnormal liver function tests (typically elevated ALT and/or AST) or hepatic steatosis on ultrasound performed for another reason. Some people report non-specific symptoms including fatigue, right upper quadrant discomfort, or malaise, but these do not correlate reliably with disease severity.

As MASLD advances to cirrhosis, complications of portal hypertension develop: ascites (abdominal fluid accumulation), variceal bleeding (oesophageal or gastric varices), hepatic encephalopathy (confusion due to liver failure), and spontaneous bacterial peritonitis. Jaundice, bruising, and coagulopathy reflect severe hepatic synthetic failure. At this stage, outcomes are poor without liver transplantation.

Diagnosing MASLD and Assessing Fibrosis

Diagnosis of hepatic steatosis is usually made by ultrasound — the liver appears bright and echogenic due to fat deposition. Ultrasound cannot reliably quantify fat or grade inflammation. Controlled attenuation parameter (CAP) on FibroScan (transient elastography), or MRI-proton density fat fraction (MRI-PDFF), provide more accurate quantification of liver fat.

Stratifying fibrosis severity is the most clinically important step — determining whether a patient is at risk of progression to cirrhosis and requires specialist input. Simple non-invasive fibrosis scores are calculated from routine clinical and laboratory data and are recommended in primary care by NICE and NHSE as the first step for all patients with suspected MASLD. The FIB-4 index (using age, AST, ALT, and platelet count) is most commonly used: FIB-4 below 1.30 — low risk of advanced fibrosis (reassure, lifestyle advice, re-test in 3 years); FIB-4 1.30–2.67 — intermediate, refer for specialist assessment; FIB-4 above 2.67 — high risk, refer urgently to hepatology.

FibroScan (liver stiffness measurement by transient elastography) is used in secondary care to assess fibrosis stage non-invasively. Liver biopsy — the gold standard for staging fibrosis and diagnosing MASH — is increasingly reserved for cases where non-invasive assessment is inconclusive and clinical management would be altered by histological diagnosis.

NHS Treatment of MASLD

There is currently no licensed drug treatment for MASLD in the UK, making lifestyle intervention the cornerstone of management. However, this is rapidly changing — resmetirom (a thyroid hormone receptor-beta agonist) was approved by the FDA in 2024 for MASH with fibrosis, and several other agents are in advanced clinical trials. NHSE is evaluating these emerging therapies.

Weight loss: The most effective intervention for MASLD. Loss of 3–5% body weight reduces liver fat. Loss of 7–10% reduces liver inflammation (MASH histology). Loss of 10% or more can reduce fibrosis stage and, in some cases, reverse early cirrhosis. Sustained weight loss of this magnitude is achievable through structured lifestyle programmes, low-calorie diets (including NHS-funded total diet replacement programmes), or bariatric surgery (which is particularly effective in achieving MASLD remission and is recommended by NICE for people with obesity-related MASLD).

Exercise: Both aerobic exercise and resistance training reduce liver fat independently of weight loss. Current recommendations include at least 150 minutes of moderate-intensity aerobic exercise plus resistance training twice weekly. Exercise also improves insulin sensitivity, metabolic syndrome, and cardiovascular risk.

Dietary advice: A Mediterranean diet (high in vegetables, legumes, wholegrains, fish, and olive oil; low in red and processed meat, refined carbohydrates, and sugar) has the strongest evidence for reducing liver fat and cardiovascular risk in MASLD. Fructose (particularly in soft drinks and fruit juices) is particularly harmful. Avoiding alcohol, even within national guidelines, is recommended for those with significant liver disease.

Managing metabolic comorbidities: Aggressive management of type 2 diabetes, hypertension, and dyslipidaemia reduces both liver and cardiovascular risk. SGLT2 inhibitors (empagliflozin, dapagliflozin) and GLP-1 receptor agonists (semaglutide, liraglutide) show benefit in reducing liver fat and inflammation in MASLD and are preferred agents for type 2 diabetes in this population. Statins are safe and recommended for cardiovascular risk reduction in MASLD — they do not worsen liver disease and may have mild hepatoprotective effects. Vitamin E (800 IU/day) has evidence for improving MASH histology in non-diabetic patients but is not currently recommended routinely due to concerns about long-term safety at high doses.

Cirrhosis management: People with MASLD-related cirrhosis require 6-monthly HCC surveillance (ultrasound ± AFP), endoscopic surveillance for varices, and management of complications. Liver transplantation is offered to eligible patients with end-stage liver disease.