Fatty spots on the liver, medically known as hepatic steatosis or non-alcoholic fatty liver disease (NAFLD), occur when excess fat accumulates within liver cells. This increasingly common condition affects an estimated 20–30% of the UK population and is closely linked to obesity, type 2 diabetes, and metabolic syndrome. Many people remain unaware they have fatty liver disease, as it often causes no symptoms in the early stages and is frequently discovered incidentally during routine scans or blood tests. Understanding this condition is essential, as whilst simple fat accumulation may be benign, a proportion of cases can progress to inflammation, scarring, and potentially serious liver complications without appropriate management and lifestyle intervention.

What Are Fatty Spots on the Liver?

Fatty spots on the liver, medically termed hepatic steatosis or non-alcoholic fatty liver disease (NAFLD), refer to the abnormal accumulation of fat within liver cells (hepatocytes). In a healthy liver, fat is present in very small amounts. Steatosis is defined as fat accumulation in 5% or more of hepatocytes (as seen on liver biopsy or MRI-based fat quantification). On ultrasound imaging, fatty liver typically appears as diffuse increased echogenicity—a generalised 'bright liver'—rather than discrete spots, though focal fatty change can occasionally occur.

The condition exists on a spectrum. Simple steatosis involves fat accumulation without significant inflammation or liver cell damage. However, a proportion of people with NAFLD—estimated at around 10–20%—may have or develop non-alcoholic steatohepatitis (NASH), where inflammation and hepatocyte injury occur alongside fat deposition. NASH carries a higher risk of advancing to liver fibrosis, cirrhosis, and potentially hepatocellular carcinoma over time.

NAFLD has become the most common chronic liver condition in the UK, affecting an estimated 20–30% of the general population. Prevalence increases significantly in individuals with obesity, type 2 diabetes, or metabolic syndrome. The condition is often discovered incidentally during imaging or blood tests performed for unrelated reasons, as many people remain asymptomatic in the early stages. (Some international guidelines now use the term metabolic dysfunction-associated steatotic liver disease [MASLD], though NAFLD remains the standard term in UK NHS and NICE guidance.)

Key points about fatty liver:

• Steatosis is defined as fat in ≥5% of hepatocytes

• Usually appears as diffuse increased echogenicity ('bright liver') on ultrasound

• Can be simple steatosis or progress to NASH

• Often asymptomatic in early stages

• Increasingly common due to rising obesity rates

Understanding the nature of fatty liver disease is essential for early intervention and preventing progression to more serious liver complications.

Causes of Fatty Liver Disease

The development of fatty liver results from complex metabolic disturbances affecting how the body processes and stores fat. The primary mechanism involves an imbalance between fat delivery to the liver, fat synthesis within hepatocytes, and the liver's capacity to export or oxidise fat. When fat accumulation exceeds the liver's processing capacity, steatosis develops.

NAFLD is diagnosed after excluding harmful alcohol intake. In the UK, harmful drinking is generally considered to exceed the Chief Medical Officers' low-risk guideline of 14 units per week. Other causes of liver disease—such as viral hepatitis, autoimmune liver disease, haemochromatosis, and medication-induced liver injury—must also be excluded.

Metabolic and lifestyle factors represent the most common causes:

• Insulin resistance and type 2 diabetes: Impaired insulin signalling promotes increased fat delivery to the liver and enhanced hepatic fat synthesis whilst reducing fat oxidation. Up to approximately 70% of people with type 2 diabetes have NAFLD.

• Obesity and excess weight: Particularly central (abdominal) adiposity strongly correlates with fatty liver development. Excess visceral fat releases free fatty acids directly into the portal circulation, overwhelming hepatic fat metabolism.

• Metabolic syndrome: The clustering of central obesity, hypertension, dyslipidaemia (elevated triglycerides, low HDL cholesterol), and insulin resistance significantly increases NAFLD risk.

• Dietary factors: Diets high in refined carbohydrates, fructose (particularly from sugar-sweetened beverages), and saturated fats contribute to hepatic fat accumulation. Excessive caloric intake regardless of composition promotes steatosis.

Other contributing factors include:

• Rapid weight loss or malnutrition (paradoxically)

• Certain medications (corticosteroids, tamoxifen, methotrexate, amiodarone, sodium valproate, some antiretroviral drugs)

• Total parenteral nutrition

• Lipodystrophy syndromes

• Polycystic ovary syndrome (PCOS)

• Hypothyroidism

• Obstructive sleep apnoea

Genetic factors also play a role, with certain gene variants (particularly PNPLA3, TM6SF2, and MBOAT7) influencing individual susceptibility to developing and progressing fatty liver disease. Understanding these causes enables targeted prevention and management strategies tailored to individual risk profiles.

Symptoms and When to See a Doctor

Fatty liver disease is often called a 'silent' condition because most people with simple steatosis experience no symptoms whatsoever. The liver has remarkable functional reserve, and early fat accumulation typically does not impair its essential metabolic, synthetic, and detoxification functions. Many individuals only discover they have fatty liver incidentally during abdominal ultrasound or blood tests performed for other reasons.

When symptoms do occur, they are usually non-specific and may include:

• Persistent fatigue or malaise: A general feeling of tiredness not explained by other factors

• Vague right upper quadrant discomfort: A dull ache or sensation of fullness beneath the right rib cage where the liver is located

• General abdominal discomfort or bloating

As the condition progresses to NASH or fibrosis, additional features may develop, though these typically indicate more advanced disease. Signs of progressive liver disease include unexplained weight loss, weakness, loss of appetite, nausea, and confusion. Advanced cirrhosis may present with jaundice (yellowing of skin and eyes), ascites (abdominal fluid accumulation), peripheral oedema, easy bruising, and spider naevi (small blood vessel clusters on the skin).

You should contact your GP if you experience:

• Persistent unexplained fatigue lasting several weeks

• Ongoing right upper abdominal discomfort

• Unexplained weight loss

• Any signs of jaundice

• Abnormal liver blood tests or incidental hepatic steatosis detected on imaging, even if you have no symptoms

• Known risk factors (obesity, diabetes, metabolic syndrome) even without symptoms

Seek urgent medical attention (call 999 or attend A&E) if you develop:

• Severe abdominal pain

• Vomiting blood or passing black, tarry stools

• Significant confusion or altered consciousness

• Marked abdominal swelling

Early detection through routine health checks is crucial, particularly for individuals with metabolic risk factors. The NHS Health Check programme (for adults aged 40–74 in England) includes assessment of cardiovascular and metabolic risk factors that overlap significantly with NAFLD risk, providing an opportunity for early identification and intervention.

Diagnosis and Tests for Fatty Liver

Diagnosing fatty liver disease involves a combination of clinical assessment, blood tests, and imaging studies. The diagnostic process aims not only to confirm steatosis but also to assess disease severity, exclude other liver conditions, and identify associated metabolic complications.

Initial assessment typically includes:

• Medical history and physical examination: Your GP will enquire about alcohol consumption (to distinguish NAFLD from alcohol-related liver disease), medications, symptoms, and risk factors. Physical examination may reveal hepatomegaly (enlarged liver) or signs of advanced disease, though examination is often normal in early stages.

• Liver function tests (LFTs): Blood tests measuring alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), bilirubin, and albumin. Elevated transaminases (particularly ALT) may indicate hepatocyte injury, though normal LFTs do not exclude fatty liver disease. The AST/ALT ratio may provide supportive information but cannot alone distinguish NAFLD from alcohol-related disease.

• Metabolic screening: Fasting glucose, HbA1c (diabetes screening), lipid profile (cholesterol and triglycerides), and assessment for metabolic syndrome components.

• Exclusion of other liver diseases: Baseline investigations should include hepatitis B surface antigen (HBsAg), hepatitis C antibody (anti-HCV), ferritin and transferrin saturation (to exclude haemochromatosis), autoimmune liver screen (antinuclear antibody [ANA], smooth muscle antibody [SMA], antimitochondrial antibody [AMA]), and coeliac serology if clinically indicated. A careful review of alcohol intake and medication history is essential.

Imaging studies provide direct visualisation:

• Ultrasound scanning: The first-line imaging modality, showing diffuse increased echogenicity ('bright liver') in steatosis. Ultrasound is widely available, non-invasive, and cost-effective, though it has limited sensitivity for detecting steatosis below 20–30% and cannot reliably distinguish simple steatosis from NASH.

• Transient elastography (FibroScan®): A specialised ultrasound technique measuring liver stiffness (indicating fibrosis) and controlled attenuation parameter (CAP score, indicating fat content). Increasingly used in secondary care for non-invasive fibrosis assessment.

• MRI-based techniques: Magnetic resonance elastography (MRE) and MRI-proton density fat fraction (MRI-PDFF) provide the most accurate non-invasive assessment of liver fat and fibrosis but are typically reserved for research or complex cases due to cost and availability.

Fibrosis assessment is crucial as fibrosis stage determines prognosis. NICE recommends using non-invasive fibrosis scores in adults with NAFLD:

• FIB-4 score: Calculated from age, AST, ALT, and platelet count. In adults aged <65 years, FIB-4 <1.3 rules out advanced fibrosis; in those aged ≥65 years, FIB-4 <2.0 rules out advanced fibrosis. FIB-4 >3.25 suggests high risk of advanced fibrosis.

• NAFLD Fibrosis Score (NFS): Incorporates age, BMI, diabetes status, AST/ALT ratio, platelet count, and albumin.

For adults with indeterminate or high fibrosis risk on initial scoring:

• Enhanced Liver Fibrosis (ELF) test: A blood test measuring three markers of fibrosis. An ELF score ≥10.51 indicates advanced fibrosis and warrants referral to hepatology.

Adults with NAFLD but without advanced fibrosis should have their fibrosis risk reassessed every 3 years using non-invasive tests.

Liver biopsy remains the gold standard for definitively diagnosing NASH and staging fibrosis but is invasive and carries small risks. It is typically reserved for cases where non-invasive tests are inconclusive or when other liver diseases need exclusion. The diagnostic approach is individualised based on clinical presentation, risk factors, and initial test results, with the goal of identifying those at higher risk of progressive disease who may benefit from closer monitoring or specialist referral.

Treatment and Lifestyle Changes

Currently, there are no medicines licensed specifically for the treatment of NAFLD in the UK. Management focuses primarily on lifestyle modification to address underlying metabolic dysfunction, prevent disease progression, and reduce cardiovascular risk. The approach is tailored to disease severity and individual circumstances.

Weight loss represents the cornerstone of treatment. Evidence demonstrates that:

• 5% weight reduction can decrease hepatic steatosis

• 7–10% weight loss can improve NASH and reduce inflammation

• ≥10% weight loss may reverse fibrosis in some individuals

Weight loss should be gradual (0.5–1 kg per week) through sustainable dietary changes and increased physical activity. Very rapid weight loss can paradoxically worsen liver inflammation.

Dietary modifications recommended include:

• Reducing overall caloric intake to achieve energy deficit

• Limiting refined carbohydrates and added sugars, particularly fructose from sugar-sweetened beverages

• Reducing saturated fat intake

• Increasing consumption of vegetables, fruits, whole grains, and lean proteins

• Following a Mediterranean-style diet pattern, which has shown particular benefit

• Avoiding fruit juices and processed foods high in added sugars

Alcohol: Even moderate alcohol consumption may be harmful in NAFLD. The UK Chief Medical Officers advise that to keep health risks from alcohol low, it is safest not to drink more than 14 units per week on a regular basis. For people with NASH or advanced fibrosis, abstinence is often recommended. Discuss your individual situation with your GP or specialist.

Physical activity provides benefits independent of weight loss:

• Aim for 150 minutes of moderate-intensity aerobic exercise weekly (brisk walking, cycling, swimming)

• Include resistance training 2–3 times weekly

• Reduce sedentary time throughout the day

• Any increase in activity is beneficial; start gradually if currently inactive

Management of associated conditions is essential:

• Diabetes control: Optimising glycaemic control through medication and lifestyle. Certain diabetes medications may provide additional metabolic benefits, but none are licensed specifically for NAFLD treatment. GLP-1 receptor agonists (such as liraglutide and semaglutide) are licensed for type 2 diabetes and obesity (where criteria are met) and should be used only for these approved indications in line with NICE guidance. Pioglitazone may be considered in adults with biopsy-proven NASH under specialist care, but it is used off-label for this purpose and carries risks including fluid retention, heart failure, and increased fracture risk; discuss benefits and risks carefully with your specialist.

• Cardiovascular risk reduction: Managing hypertension and dyslipidaemia is crucial. Statins are safe and effective in people with NAFLD when indicated for cardiovascular risk reduction. Antiplatelet therapy may be prescribed where appropriate. Cardiovascular disease represents the leading cause of mortality in people with NAFLD.

• Obstructive sleep apnoea treatment: Continuous positive airway pressure (CPAP) therapy where indicated, as sleep apnoea independently worsens NAFLD.

Vitamin E (high-dose, 800 IU daily) has shown benefit in some adults with biopsy-proven NASH who do not have diabetes, but it is not routinely recommended due to potential long-term safety concerns (including signals of increased risk of haemorrhagic stroke and prostate cancer). It should only be considered under specialist supervision and is used off-label.

Vaccination: People with chronic liver disease, including those with advanced fibrosis or cirrhosis, should be offered vaccination against hepatitis A and hepatitis B in line with UK guidance.

Monitoring and follow-up depends on disease severity:

• Adults with NAFLD but without advanced fibrosis: Reassess fibrosis risk every 3 years using non-invasive tests; monitor and manage metabolic risk factors (diabetes, hypertension, dyslipidaemia) as part of routine care.

• Advanced fibrosis (F3) or cirrhosis: Specialist hepatology follow-up. In cirrhosis, surveillance for hepatocellular carcinoma (6-monthly ultrasound ± alpha-fetoprotein) and variceal screening (endoscopy) are recommended in line with NICE guidance. Decisions about surveillance in advanced fibrosis without cirrhosis are made on an individual basis.

Bariatric surgery may be considered for individuals with obesity (BMI ≥35 kg/m² with comorbidities, or ≥40 kg/m²) and NAFLD who have not achieved adequate weight loss through lifestyle measures, following NICE guidance on obesity management.

Reporting side effects: If you experience any side effects from medicines or supplements, you can report them via the MHRA Yellow Card scheme at https://yellowcard.mhra.gov.uk or by searching for 'Yellow Card' in the Google Play or Apple App Store.

Patient education and support are vital for achieving sustainable lifestyle changes. Referral to dietitians, diabetes specialist nurses, or weight management services can provide structured support. Regular follow-up helps maintain motivation and allows monitoring of disease progression and cardiovascular risk factors. The prognosis for NAFLD is generally favourable with appropriate management, particularly when intervention occurs before significant fibrosis develops.

Frequently Asked Questions