Can a fatty liver cause high bilirubin? This question concerns many people diagnosed with fatty liver disease who notice abnormal blood test results. Whilst simple fatty liver (steatosis) typically does not elevate bilirubin levels, the answer depends on disease severity. In most cases, bilirubin remains normal even with fat accumulation in the liver. However, when fatty liver progresses to inflammation (steatohepatitis) and advanced scarring (cirrhosis), the liver's ability to process bilirubin becomes impaired, potentially causing elevated levels and jaundice. Understanding this relationship helps patients recognise when liver disease may be advancing and requires closer medical attention.

Understanding Fatty Liver Disease and Bilirubin Levels

Fatty liver disease, medically termed hepatic steatosis, occurs when excess fat accumulates within liver cells. This condition exists in two main forms: non-alcoholic fatty liver disease (NAFLD), which affects individuals who drink little or no alcohol, and alcohol-related liver disease (ARLD), which develops due to excessive alcohol consumption. NAFLD has become increasingly common in the UK, affecting approximately one in three adults according to NHS data, often associated with obesity, type 2 diabetes, and metabolic syndrome. This prevalence figure largely refers to early-stage steatosis detected on imaging or blood tests.

Bilirubin is a yellow-orange pigment produced during the normal breakdown of red blood cells. When red blood cells reach the end of their lifespan (approximately 120 days), they are broken down by the spleen and other tissues, releasing haemoglobin. This haemoglobin is converted into bilirubin, which then travels to the liver bound to albumin. The liver plays a crucial role in processing bilirubin by conjugating it (making it water-soluble) through the enzyme UDP-glucuronosyltransferase 1A1 (UGT1A1) and excreting it into bile, which eventually leaves the body through the digestive system.

Normal bilirubin levels in adults typically range from 3 to 17 micromoles per litre (µmol/L) for total bilirubin, though reference ranges may vary slightly between laboratories. When bilirubin levels rise above normal ranges, a condition called hyperbilirubinaemia develops, which may manifest as jaundice—a yellowing of the skin and whites of the eyes. Understanding the relationship between liver health and bilirubin metabolism is essential, as the liver's ability to process bilirubin effectively depends on its functional capacity. Any condition affecting liver cells, including fatty liver disease, has the potential to disrupt this delicate balance, though the extent varies considerably depending on disease severity and progression.

Can a Fatty Liver Cause High Bilirubin?

In most cases of simple fatty liver disease (steatosis alone), bilirubin levels remain within normal ranges. The accumulation of fat within liver cells (hepatocytes) does not typically impair the liver's ability to process bilirubin sufficiently to cause clinically significant elevation. Many individuals with NAFLD have completely normal liver function tests, including bilirubin measurements, particularly in the early stages of the condition. This is because the liver possesses substantial functional reserve, and mild to moderate fat accumulation alone does not usually compromise its metabolic capacity.

When fatty liver disease progresses to non-alcoholic steatohepatitis (NASH)—characterised by inflammation and liver cell damage alongside fat accumulation—the situation may change, though bilirubin typically remains normal until disease is advanced. NASH represents a more severe form of fatty liver disease where ongoing inflammation causes hepatocyte injury and death. However, sustained elevation of bilirubin in someone with known fatty liver disease should prompt assessment for alternative causes or progression to advanced fibrosis or cirrhosis, as NASH alone rarely raises bilirubin unless complicated by cholestasis or significant fibrosis.

Advanced liver disease resulting from long-standing fatty liver disease presents the greatest risk for elevated bilirubin. When NASH progresses to liver fibrosis and eventually cirrhosis (severe scarring), significant portions of functional liver tissue are replaced by scar tissue. At this stage, the liver's capacity to perform its normal functions, including bilirubin processing, becomes substantially compromised. Patients with cirrhosis secondary to NAFLD may develop jaundice and markedly elevated bilirubin levels, indicating advanced liver dysfunction.

It is important to note that other causes of raised bilirubin are common and should be considered. These include:

• Gilbert's syndrome—a benign inherited condition causing intermittent mild unconjugated hyperbilirubinaemia, affecting approximately 5% of the UK population, with otherwise normal liver function tests

• Biliary obstruction from gallstones, strictures, or tumours, typically causing conjugated hyperbilirubinaemia with dark urine and pale stools

• Haemolysis (increased red blood cell breakdown), causing unconjugated hyperbilirubinaemia

• Viral or autoimmune hepatitis, drug-induced liver injury, and other liver diseases

When bilirubin is elevated, your doctor will typically request fractionation (measuring direct/conjugated and indirect/unconjugated bilirubin) to help identify the underlying cause. Therefore, whilst simple fatty liver rarely causes high bilirubin, progressive disease with advanced fibrosis or cirrhosis can indeed result in elevated levels, serving as an important marker of disease severity and liver functional impairment.

How Fatty Liver Affects Liver Function and Bilirubin Processing

The liver performs over 500 vital functions, with bilirubin metabolism representing just one aspect of its complex biochemical repertoire. In healthy liver tissue, hepatocytes efficiently take up unconjugated (indirect) bilirubin from the bloodstream, conjugate it with glucuronic acid through the enzyme UDP-glucuronosyltransferase 1A1 (UGT1A1), and excrete the conjugated (direct) bilirubin into bile canaliculi. This process requires intact cellular machinery, adequate enzyme function, and unobstructed bile flow.

When fat accumulates within hepatocytes in fatty liver disease, it occupies cellular space and can interfere with normal metabolic processes. In simple steatosis, however, this interference is generally minimal, and the liver compensates effectively. The hepatocytes remain viable and functional despite fat accumulation, maintaining adequate bilirubin processing capacity. Routine liver function tests, including bilirubin, often remain normal, though other markers such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), and occasionally alkaline phosphatase (ALP) may show mild elevation. A predominantly hepatocellular pattern (raised ALT/AST) is typical of NAFLD, whereas a cholestatic pattern (raised ALP/GGT) suggests biliary disease and warrants further investigation.

The transition to NASH introduces a critical pathophysiological change. Inflammation triggers oxidative stress and cellular injury, leading to hepatocyte death (apoptosis and necrosis). As liver cells die, their capacity to process bilirubin diminishes. Cholestasis (impaired bile flow) can occasionally occur in NASH but is less common than in primary biliary or obstructive disorders. When cholestasis does develop, conjugated bilirubin cannot be efficiently excreted into bile and instead accumulates in the bloodstream, causing elevated direct bilirubin levels. Any cholestatic picture warrants evaluation for biliary obstruction, primary biliary cholangitis, primary sclerosing cholangitis, and drug-induced liver injury.

In advanced fibrosis and cirrhosis, architectural distortion of the liver becomes pronounced. Fibrous scar tissue replaces functional hepatocytes, and the normal lobular structure is disrupted. Blood flow through the liver becomes compromised due to increased resistance, and the remaining hepatocytes struggle to maintain metabolic functions. At this stage, both unconjugated and conjugated bilirubin may accumulate, reflecting the liver's severely diminished functional capacity. According to NICE guidance (NG50: Cirrhosis in over 16s), patients with cirrhosis require regular monitoring of liver function, including bilirubin levels, as part of comprehensive disease management. Non-invasive tests such as transient elastography (FibroScan) are increasingly used to assess liver stiffness and stage fibrosis, helping to identify those at risk of progression.

Symptoms and Signs of Elevated Bilirubin with Fatty Liver

Mild elevations in bilirubin often produce no noticeable symptoms, and many individuals remain unaware of the abnormality until blood tests are performed. This asymptomatic phase is common in early liver disease, emphasising the importance of risk-based assessment, particularly for individuals with risk factors such as obesity, diabetes, or metabolic syndrome.

As bilirubin levels rise, jaundice becomes the most recognisable clinical sign. Scleral icterus (yellowing of the whites of the eyes) is typically visible when bilirubin reaches approximately 35–50 µmol/L, though this threshold varies between individuals and lighting conditions. Jaundice manifests as:

• Yellowing of the skin and mucous membranes, typically first noticeable in good natural light

• Scleral icterus—yellowing of the whites of the eyes, often the earliest visible sign

• Dark urine resembling tea or cola, caused by excess conjugated bilirubin being excreted by the kidneys

• Pale or clay-coloured stools, resulting from reduced bilirubin reaching the intestines

• Pruritus (itching), which can be severe and distressing, caused by bile salt accumulation in the skin

Dark urine and pale stools strongly suggest conjugated hyperbilirubinaemia and possible biliary obstruction, warranting urgent assessment to exclude gallstones, strictures, or other obstructive causes.

When elevated bilirubin occurs in the context of progressive fatty liver disease, patients may experience additional symptoms reflecting underlying liver dysfunction:

• Fatigue and weakness, often profound and limiting daily activities

• Abdominal discomfort or pain in the right upper quadrant where the liver is located

• Loss of appetite and unintentional weight loss

• Nausea and general malaise

• Easy bruising or bleeding, indicating impaired synthesis of clotting factors

In advanced liver disease with significantly elevated bilirubin, more serious complications may develop, including hepatic encephalopathy (confusion and altered consciousness due to toxin accumulation), ascites (fluid accumulation in the abdomen), and peripheral oedema (leg swelling). These features indicate decompensated cirrhosis and require urgent medical attention. It is important to note that many individuals with fatty liver disease and even early cirrhosis may have minimal symptoms, making regular medical monitoring essential for those with known liver conditions.

When to Seek Medical Advice for Liver Health Concerns

Immediate medical attention is warranted if you develop jaundice (yellowing of the skin or eyes), as this always requires investigation to determine the underlying cause. Whilst jaundice can result from various conditions—including bile duct obstruction, haemolytic disorders, or liver disease—it represents a significant abnormality that demands prompt evaluation. Contact your GP urgently, call NHS 111 for advice, or attend an emergency department (A&E) if jaundice is accompanied by severe abdominal pain (especially right upper quadrant), fever, confusion, or vomiting. These features may indicate cholangitis (bile duct infection), biliary obstruction, or decompensated liver disease requiring urgent treatment.

You should arrange a routine GP appointment if you experience:

• Persistent fatigue that affects your daily functioning

• Unexplained weight loss or loss of appetite

• Ongoing abdominal discomfort, particularly in the right upper abdomen

• Dark urine or pale stools persisting for more than a few days

• Unusual bruising or bleeding tendencies

• Persistent itching without an obvious skin cause

Individuals with known risk factors for fatty liver disease should discuss liver health assessment with their GP. Risk factors include obesity (particularly central adiposity), type 2 diabetes, high cholesterol or triglycerides, metabolic syndrome, and a history of excessive alcohol consumption. UK practice follows a risk-based approach rather than population screening. According to NICE guidance (NG49: Non-alcoholic fatty liver disease), patients with suspected or confirmed NAFLD should undergo risk stratification using validated scores such as the FIB-4 score or NAFLD fibrosis score. If these scores are indeterminate or suggest advanced fibrosis, further assessment with the Enhanced Liver Fibrosis (ELF) blood test and/or transient elastography (FibroScan) may be arranged. Retesting intervals depend on fibrosis risk; adults with low-risk scores typically do not require retesting more often than every three years, whilst those with intermediate or high risk require closer monitoring and may be referred to hepatology services.

If you have been diagnosed with fatty liver disease, maintain regular follow-up appointments as recommended by your healthcare team. Report any new symptoms promptly, as these may indicate disease progression. Your GP may arrange blood tests (including liver function tests with bilirubin measurement), liver ultrasound, or specialist referral to hepatology services depending on your clinical picture and fibrosis risk stratification.

Lifestyle modifications remain the cornerstone of managing fatty liver disease and preventing progression. Evidence-based interventions include:

• Weight loss: Losing ≥7–10% of body weight can improve NASH; weight loss of ≥10% may lead to regression of fibrosis

• Regular physical activity: Aim for at least 150 minutes of moderate-intensity exercise per week

• Balanced diet: A Mediterranean-style diet rich in vegetables, fruits, whole grains, oily fish, and healthy fats is recommended

• Alcohol limits: Follow UK Chief Medical Officers' low-risk drinking guidelines—no more than 14 units per week, spread over three or more days, with several alcohol-free days each week

• Optimise management of diabetes, high blood pressure, and cholesterol

The NHS provides resources and support services for weight management, alcohol reduction, and diabetes care that can benefit liver health. Early intervention, risk stratification, and regular monitoring offer the best opportunity to prevent complications and maintain liver function over the long term.

Frequently Asked Questions