Does fatty liver cause low albumin? This is a common concern for patients diagnosed with hepatic steatosis. Simple fatty liver disease alone does not typically cause low albumin levels. In early-stage non-alcoholic fatty liver disease (NAFLD) or alcohol-related liver disease (ARLD), the liver's ability to produce albumin—the most abundant blood protein—remains intact. Low albumin levels generally emerge only when fatty liver progresses to advanced stages such as cirrhosis, where extensive scarring impairs the liver's synthetic function. Understanding this relationship helps patients recognise when fatty liver requires closer monitoring and when other causes of low albumin should be investigated.

Understanding Fatty Liver Disease and Albumin 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 includes fatty change in people who drink above recommended limits. NAFLD has become increasingly common in the UK, affecting around a quarter to a third of adults, often associated with obesity, type 2 diabetes, and metabolic syndrome.

Albumin is the most abundant protein in human blood plasma, synthesised exclusively by the liver. This essential protein performs several critical functions: it maintains oncotic pressure (keeping fluid within blood vessels), transports hormones, vitamins, and medications throughout the body, and serves as a marker of the liver's synthetic function. Normal serum albumin levels typically range between 35–50 g/L in adults, though reference ranges may vary slightly between laboratories.

Albumin levels primarily reflect the liver's ability to produce proteins and respond to inflammation. Importantly, albumin is a negative acute-phase reactant—its levels fall during inflammation and acute illness—and is not a reliable marker of nutritional status alone. When liver cells become damaged or their function deteriorates, albumin production may decline, leading to hypoalbuminaemia (low albumin levels). Understanding the relationship between fatty liver disease and albumin levels is important because it helps patients and healthcare professionals assess disease severity and progression.

In the early stages of fatty liver disease, liver function typically remains preserved, and albumin levels usually stay within normal range. It is important to note that normal liver blood tests do not exclude significant liver scarring (fibrosis) in NAFLD. However, as the condition progresses—particularly if inflammation develops (steatohepatitis) or scarring occurs (fibrosis)—the liver's ability to synthesise proteins including albumin may become compromised. This progression is not inevitable, and many people with fatty liver disease maintain normal liver function throughout their lives with appropriate lifestyle modifications.

Does Fatty Liver Cause Low Albumin?

Simple fatty liver disease alone does not typically cause low albumin levels. In the early stages of NAFLD or ARLD, when fat accumulation occurs without significant inflammation or scarring, the liver's synthetic function remains intact. Most patients with uncomplicated fatty liver disease will have albumin levels within the normal reference range, and routine blood tests may show entirely normal results.

The relationship between fatty liver and low albumin becomes clinically relevant only when the disease progresses to more advanced stages. When fatty liver advances to non-alcoholic steatohepatitis (NASH)—characterised by inflammation and liver cell injury—or develops significant fibrosis (scarring), the liver's functional capacity begins to decline. Even at these stages, albumin levels may remain normal until substantial liver damage has occurred. It is important to remember that normal liver enzyme levels (ALT and AST) do not rule out the presence of fibrosis, so additional assessment may be needed.

Low albumin levels typically emerge when fatty liver disease progresses to cirrhosis—the advanced stage where extensive scarring replaces healthy liver tissue. Cirrhosis represents end-stage liver disease, where the liver's architecture becomes severely disrupted and its ability to perform essential functions, including albumin synthesis, becomes significantly impaired. At this stage, albumin levels often fall below the normal range, and patients may develop complications such as ascites (fluid accumulation in the abdomen) and peripheral oedema.

It is important to emphasise that the progression from simple fatty liver to cirrhosis is neither rapid nor inevitable. Studies suggest that a minority of people with NAFLD will develop NASH, and a smaller proportion will progress to cirrhosis, though individual risk varies depending on factors such as diabetes, obesity, and age. The timeframe for such progression typically spans many years or decades. Therefore, if you have been diagnosed with fatty liver disease and have low albumin levels, your GP will investigate other potential causes, as the fatty liver alone is unlikely to be responsible unless advanced liver disease is present.

Seek urgent medical attention if you develop signs of liver decompensation, including jaundice (yellowing of skin or eyes) with feeling unwell, abdominal swelling, confusion or altered behaviour, vomiting blood, or black tarry stools. These symptoms require same-day assessment or emergency care.

Other Causes of Low Albumin to Consider

When low albumin is detected, healthcare professionals must consider numerous potential causes beyond liver disease. Low albumin is often multifactorial, and several conditions may contribute simultaneously.

Malnutrition and inadequate protein intake can contribute to low albumin, particularly in elderly patients, those with eating disorders, or individuals following severely restricted diets. However, albumin is not a reliable marker of nutritional status alone, as it is also affected by inflammation and other factors. The body requires adequate dietary protein to synthesise albumin, and severe chronic nutritional deficiency may contribute to reduced levels.

Kidney disease, specifically nephrotic syndrome, causes significant albumin loss through urine (proteinuria). The kidneys' filtering units become damaged, allowing albumin to leak from the bloodstream into urine. Patients may notice foamy urine, swelling around the eyes, and ankle oedema. Chronic kidney disease of any cause can also contribute to low albumin through multiple mechanisms including reduced synthesis and increased breakdown.

Inflammatory conditions and chronic diseases frequently cause low albumin levels. During acute or chronic inflammation, the body's protein metabolism shifts, reducing albumin production whilst increasing synthesis of acute-phase proteins. Conditions such as rheumatoid arthritis, inflammatory bowel disease (Crohn's disease or ulcerative colitis), chronic infections, and malignancies can all suppress albumin levels. This phenomenon occurs even when liver and kidney function remain normal.

Protein-losing enteropathy—where protein is lost through the gastrointestinal tract—can result from conditions including coeliac disease, intestinal lymphangiectasia, or severe inflammatory bowel disease. Heart failure may cause low albumin through multiple mechanisms including liver congestion, reduced synthesis, and increased breakdown. Severe burns, major surgery, or critical illness cause albumin to leak from blood vessels into tissues and increase protein breakdown.

Fluid overload (haemodilution) can dilute albumin concentration, and pregnancy physiologically reduces albumin levels. Given these diverse causes, comprehensive assessment is essential when hypoalbuminaemia is identified, rather than attributing it solely to fatty liver disease.

Testing and Monitoring Albumin Levels

Albumin levels are typically measured as part of a liver function test (LFT) panel, which also includes enzymes such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and bilirubin. Your GP may request LFTs for various reasons: investigating symptoms, monitoring known liver conditions, checking medication side effects, or as part of routine health screening. The test requires a simple blood sample, usually taken from a vein in your arm, and results are typically available within a few days.

When interpreting albumin results, healthcare professionals consider the clinical context and compare values against your local laboratory's reference range. Low albumin may indicate liver disease, kidney disease, inflammation, or other conditions, and further investigation is guided by your symptoms, medical history, and other blood test results. Normal liver blood tests do not exclude significant liver fibrosis in people with NAFLD, so additional assessment may be needed.

For patients with diagnosed fatty liver disease, NICE guidance (NG49) recommends a structured approach to assessment and monitoring based on fibrosis risk rather than routine annual liver function tests. In primary care, your GP should use a non-invasive fibrosis risk score such as the FIB-4 score or NAFLD fibrosis score, which incorporate age, liver enzymes, and platelet count to estimate the likelihood of advanced fibrosis. If the score suggests indeterminate or high risk, your GP may arrange an enhanced liver fibrosis (ELF) blood test for further assessment. High-risk results should prompt referral to a liver specialist (hepatologist). For adults with NAFLD at low risk of advanced fibrosis, fibrosis risk assessment should be repeated approximately every three years, or sooner if clinical circumstances change.

Additional investigations may include:

• Kidney function tests (urea and electrolytes, or U&Es) to assess kidney function

• Bone profile to check calcium, phosphate, and alkaline phosphatase

• Urinalysis to check for protein loss through kidneys

• Inflammatory markers (CRP, ESR) if inflammatory conditions are suspected

• Liver imaging (ultrasound, FibroScan, or MRI) to assess liver structure and fat content

• Liver biopsy in selected cases where diagnosis remains uncertain or disease severity needs confirmation

If you have concerns about your albumin levels or liver function, discuss them with your GP, who can interpret results in the context of your overall health and arrange appropriate follow-up. Your GP will also determine whether referral to a liver specialist is needed based on your fibrosis risk assessment and other clinical factors.

Managing Fatty Liver to Protect Liver Function

The cornerstone of fatty liver disease management involves lifestyle modification, which can halt disease progression and, in many cases, reverse fat accumulation. There are currently no medicines licensed specifically to treat NAFLD in the UK, making lifestyle interventions the primary therapeutic approach recommended by NICE.

Weight loss represents the most effective intervention for NAFLD. Evidence demonstrates that losing 7–10% of body weight can significantly reduce liver fat, inflammation, and even fibrosis. This should be achieved gradually through sustainable dietary changes and increased physical activity, aiming for 0.5–1 kg weight loss per week. Crash diets or rapid weight loss may paradoxically worsen liver inflammation and should be avoided. Your GP may refer you to a weight-management service for structured support. For people who meet specific criteria (such as a BMI ≥35 kg/m² with NAFLD-related complications), NICE-recommended weight-management options may include pharmacotherapy or, in selected cases, referral for consideration of bariatric surgery.

Dietary modifications should focus on:

• Reducing intake of refined carbohydrates, added sugars, and sugar-sweetened beverages

• Limiting saturated fats whilst incorporating healthy fats from sources like olive oil, nuts, and oily fish

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

• Following a Mediterranean-style diet, which has demonstrated benefits for liver health

• Avoiding excessive fructose from fruit juices and processed foods

Regular physical activity benefits liver health independently of weight loss. UK guidance recommends at least 150 minutes of moderate-intensity aerobic activity weekly, such as brisk walking, cycling, or swimming. Both aerobic exercise and resistance training have shown benefits for reducing liver fat.

Managing associated conditions is crucial. Optimising control of type 2 diabetes, hypertension, and dyslipidaemia reduces cardiovascular risk, which is the leading cause of death in people with NAFLD. Your GP may prescribe medications such as metformin for diabetes or statins for high cholesterol. These medicines are used for their licensed indications (controlling blood sugar and cholesterol levels) and are safe in people with fatty liver disease. They are not prescribed to treat NAFLD itself, though good control of diabetes and cholesterol is important for overall health.

Alcohol consumption should follow UK Chief Medical Officers' guidance: to keep health risks from alcohol low, it is safest not to drink more than 14 units per week on a regular basis, and if you do drink this amount, spread it over three or more days. For people with any degree of liver fibrosis, cirrhosis, or alcohol-related liver disease, abstinence is advisable. Your GP or liver specialist will provide personalised advice based on your individual circumstances.

Avoiding hepatotoxic substances protects remaining liver function. This includes being cautious with medications such as paracetamol (not exceeding recommended doses), avoiding unnecessary supplements (particularly high-dose vitamin A), and discussing all medications and herbal remedies with your GP or pharmacist. If you experience a suspected side effect from any medicine, you can report it via the MHRA Yellow Card scheme at yellowcard.mhra.gov.uk or through the Yellow Card app.

Vaccination against hepatitis A and hepatitis B is recommended for people with chronic liver disease, as these infections can cause additional liver damage. Speak to your GP about whether you need these vaccinations.

When to seek medical attention: Contact your GP if you develop symptoms suggesting liver disease progression, including persistent fatigue, unexplained weight loss, or new symptoms. Seek urgent same-day assessment or emergency care if you develop jaundice (yellowing of skin or eyes) with feeling unwell, abdominal swelling, confusion or altered behaviour, unexplained bruising or bleeding, vomiting blood, or black tarry stools. Regular monitoring and early detection of disease progression enable timely intervention to preserve liver function and prevent complications including low albumin levels.

Frequently Asked Questions