Liver function tests (LFTs) are one of the most commonly ordered blood panels in Australian pathology. They appear on your results as a cluster of markers — ALT, AST, GGT, ALP, albumin, bilirubin, total protein — that together give a picture of how your liver is performing. But most people receive their results with little explanation of what each number actually means, why it matters, or what patterns to watch for over time. This guide covers every marker in a standard liver panel, the calculated ratios clinicians use to interpret them, what abnormal results may indicate, and how to have a more informed conversation with your GP.
What is a liver function test?
A liver function test is a group of blood tests ordered together to assess liver health. In Australia, pathology forms often abbreviate the panel as "LFTs" — you may see this term on a referral or printed at the top of a results section.
Despite the name, not every marker in the panel directly measures liver function. Some measure liver cell damage. Others measure substances the liver produces. The combination gives your GP a more complete picture than any single marker could.
A standard Australian liver function panel typically includes:
- ALT (alanine transaminase) — a liver enzyme released when liver cells are stressed or damaged
- AST (aspartate transaminase) — an enzyme found in the liver, heart, and muscle
- GGT (gamma-glutamyl transferase) — sensitive to alcohol, medications, and bile duct problems
- ALP (alkaline phosphatase) — related to bile ducts and bone metabolism
- Albumin — a protein synthesised by the liver; reflects long-term liver function
- Total bilirubin — a breakdown product of red blood cells, processed by the liver
- Total protein — the combined level of albumin and globulin in the blood
LFTs are one of the most frequently requested tests in Australian general practice. They are routinely ordered during annual health checks, when monitoring medications, and when investigating symptoms like fatigue, abdominal discomfort, or unexplained weight changes.
What your liver actually does
The liver is the largest internal organ in your body and one of the most metabolically active. It performs over 500 distinct functions — far more than most people realise.
Think of the liver less as a filter and more as a central processing hub. Everything you eat, drink, or absorb passes through it before reaching systemic circulation. The liver decides what to store, what to convert, what to neutralise, and what to send out to the rest of the body.
Its core roles include:
- Metabolism — converting carbohydrates, fats, and proteins into usable energy and building blocks
- Detoxification — breaking down alcohol, medications, and metabolic waste products into forms the body can excrete
- Protein synthesis — producing albumin (which maintains blood volume and transports hormones), clotting factors, and immune proteins
- Bile production — manufacturing bile to emulsify dietary fats for absorption in the small intestine
- Glycogen storage — storing glucose as glycogen and releasing it between meals to stabilise blood sugar
- Hormone regulation — processing and clearing hormones like oestrogen, cortisol, and thyroid hormones
- Vitamin and mineral storage — holding reserves of vitamins A, D, E, K, B12, and iron
Because the liver is central to so many systems, disruption to its function can produce symptoms far removed from the abdomen — fatigue, hormonal imbalance, skin changes, poor sleep, and impaired immunity can all have liver-related contributors.
The key biomarkers in your liver panel
ALT (Alanine Transaminase)
ALT is an enzyme found predominantly in liver cells. When liver cells are inflamed, injured, or under metabolic stress, ALT leaks into the bloodstream — making it a sensitive and relatively liver-specific marker of liver cell damage.
Australian reference ranges vary by laboratory and sex. Most Australian labs report an upper limit of approximately 35–45 U/L for women and 50–56 U/L for men, though published research suggests optimal levels may be lower — closer to 25–30 U/L for women and 33–40 U/L for men (Valenti et al., Hepatology Communications, 2021; Tan et al., Alimentary Pharmacology and Therapeutics, 2024). Discuss what range applies to your specific pathology report with your GP.
Elevated ALT is one of the earliest signs of fatty liver disease, alcohol-related liver injury, and viral hepatitis. Mildly elevated ALT (up to five times the upper limit of normal) is common and has many causes. Very high ALT (more than 10–20 times the upper limit) points toward acute liver injury.
AST (Aspartate Transaminase)
AST is found in liver cells but also in heart muscle, skeletal muscle, kidneys, and red blood cells. It is less liver-specific than ALT — which means elevated AST can come from sources other than the liver.
Typical Australian reference range: up to 35–40 U/L (some labs go to 45 U/L for men). AST alone is rarely diagnostic, but its relationship to ALT provides important context — particularly via the De Ritis ratio, discussed below.
Isolated AST elevation without ALT elevation often points toward muscle injury rather than liver disease. When both are elevated, the liver is the more likely source.
GGT (Gamma-Glutamyl Transferase)
GGT is an enzyme involved in glutathione metabolism and amino acid transport. It is present in the liver, bile ducts, kidneys, and pancreas. GGT is highly sensitive to alcohol intake and certain medications, and it rises early in bile duct obstruction.
Reference range: approximately 8–61 U/L for men and 8–36 U/L for women (varies by lab). Even moderate, regular alcohol consumption can raise GGT significantly — it is one of the most reliable biological indicators of alcohol intake.
Isolated GGT elevation (with normal ALP and bilirubin) most commonly reflects alcohol use or medication effects. When GGT is elevated alongside ALP, it points toward bile duct or cholestatic disease rather than bone disease.
ALP (Alkaline Phosphatase)
ALP is an enzyme found in the liver, bile ducts, bone, intestine, and placenta. It rises in two main contexts: bile duct obstruction (cholestatic liver disease) and increased bone turnover.
Reference range: approximately 30–120 U/L for adults (higher in children and pregnant women, where bone and placental sources contribute). A key interpretive question with elevated ALP is whether the source is hepatic or bone-related — GGT can help distinguish the two, as bone-derived ALP does not raise GGT.
Significant ALP elevation alongside elevated GGT and bilirubin suggests cholestatic disease — bile duct obstruction, primary biliary cholangitis, or other hepatobiliary conditions.
Albumin
Albumin is the most abundant protein in blood, synthesised exclusively by the liver. It serves as a carrier protein for hormones, fatty acids, and medications, and maintains oncotic pressure — the force that keeps fluid inside blood vessels.
Reference range: 35–50 g/L. Albumin has a relatively long half-life (approximately 20 days), so it is not a sensitive marker of acute liver injury. It is, however, a strong indicator of chronic liver function — levels fall progressively in cirrhosis, chronic malnutrition, and severe inflammatory states.
Low albumin in the context of other abnormal LFTs is a concerning pattern suggesting reduced liver synthetic function. Low albumin with normal LFTs may point toward malnutrition, nephrotic syndrome, or chronic inflammation.
Total Bilirubin
Bilirubin is the yellow-orange breakdown product of haemoglobin from aged red blood cells. The liver takes up bilirubin from the blood, conjugates it, and excretes it into bile. Elevated bilirubin causes jaundice — yellowing of the skin and whites of the eyes.
Reference range: 2–20 µmol/L. Mild isolated bilirubin elevation (up to around 35–40 µmol/L) is common and often benign — particularly in Gilbert's syndrome, a harmless genetic variant affecting an estimated 5–10% of the general population (Kwo et al., American Journal of Gastroenterology, 2017) where bilirubin clearance is mildly impaired.
Significant bilirubin elevation alongside elevated ALP and GGT suggests bile duct obstruction. Elevated bilirubin alongside elevated ALT and AST points toward liver cell damage. The pattern matters as much as the number.
Total Protein
Total protein measures the combined level of albumin and globulin in the blood. Albumin is liver-derived; globulin is largely produced by the immune system. The ratio between them (albumin-globulin ratio) carries diagnostic significance.
Reference range: 60–80 g/L. Low total protein can reflect reduced albumin production (chronic liver disease, malnutrition) or protein loss (kidney disease, malabsorption). Elevated total protein may indicate elevated globulins, which can be associated with chronic inflammation, autoimmune conditions, or plasma cell disorders.
Calculated ratios that add context
Individual biomarker levels tell part of the story. Calculated ratios tell you how those markers relate to each other — and that relationship is often more informative than any single number.
De Ritis Ratio (AST:ALT)
The De Ritis ratio divides AST by ALT. In most liver diseases, ALT is proportionally higher than AST, giving a ratio below 1. When AST exceeds ALT (ratio above 2), it suggests alcohol-related liver disease or advanced liver fibrosis — conditions where liver cell architecture is disrupted enough to release proportionally more AST.
A De Ritis ratio above 2 alongside elevated GGT is a strong signal for alcohol-related liver injury. The ratio is also used as a prognostic marker in liver disease staging.
GGT:ALT Ratio
The GGT:ALT ratio helps distinguish between alcohol-related liver disease and non-alcoholic fatty liver disease. In alcohol-related liver disease, GGT is disproportionately elevated relative to ALT. In NAFLD, GGT rises more modestly.
A GGT:ALT ratio above 1.5–2.0 in the context of elevated transaminases raises suspicion for an alcohol contribution, even in patients who minimise their drinking history.
Albumin-Globulin Ratio
The albumin-globulin ratio is derived from total protein and albumin. A low ratio (below 1.0) suggests either reduced albumin synthesis (liver disease) or elevated globulins (chronic inflammation, autoimmune disease, multiple myeloma). A high ratio is generally less clinically significant.
In chronic liver disease, the albumin-globulin ratio often inverts as albumin production falls and globulins rise in response to systemic inflammation.
Bilirubin-to-Albumin Ratio
The bilirubin-to-albumin ratio reflects the balance between bilirubin production and liver clearance capacity. In advanced liver disease, as albumin production falls and bilirubin clearance becomes impaired, this ratio rises. It is used as a marker of liver functional reserve in clinical settings.
The Globulin Gap
The globulin gap is calculated by subtracting albumin from total protein. It provides an estimate of globulin levels when direct globulin measurement is not available. A persistently elevated globulin gap (above 18 g/L) warrants investigation for autoimmune conditions, chronic infections, or plasma cell disorders.
Non-alcoholic fatty liver disease and what your liver tests reveal
Non-alcoholic fatty liver disease (NAFLD) — now increasingly referred to as metabolic dysfunction-associated steatotic liver disease (MASLD) — is the most common liver condition in Australia. According to the Gastroenterological Society of Australia (GESA), fatty liver disease affects more than 1 in 3 Australians.
NAFLD encompasses a spectrum:
- Simple steatosis — fat accumulation in liver cells without significant inflammation. ALT may be mildly elevated or normal.
- Non-alcoholic steatohepatitis (NASH/MASH) — fat plus inflammation. ALT and AST are more consistently elevated.
- Fibrosis — progressive scarring of liver tissue. The De Ritis ratio may begin to rise as fibrosis advances.
- Cirrhosis — end-stage scarring. Albumin falls, bilirubin rises, and the synthetic capacity of the liver is compromised.
The condition is closely linked to metabolic risk factors: obesity, central adiposity (waist circumference), insulin resistance, type 2 diabetes, high triglycerides, and low HDL cholesterol. Many people with NAFLD have blood test results that fall within the conventional reference range — which is why conventional ranges are not always sufficient to catch early changes.
Which LFT markers shift first in NAFLD? ALT typically rises before AST in early metabolic fatty liver. GGT also rises with progressive metabolic strain. Crucially, a normal LFT result does not rule out fatty liver — up to 30% of people with confirmed fatty liver on imaging may have ALT levels within the standard reference range.
This is why NAFLD is frequently identified incidentally on ultrasound rather than through blood tests alone. If you have risk factors — particularly metabolic syndrome or central obesity — raising the question with your GP is worthwhile even if your LFTs appear normal.
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Start Testing TodayCommon causes of abnormal liver function results
Abnormal LFTs are common and have a wide range of causes. Most mild elevations are benign and reversible. Here are the most frequently encountered explanations.
Alcohol
Alcohol is one of the most common causes of elevated GGT, AST, and ALT in Australian adults. Even moderate regular drinking raises GGT. The De Ritis ratio above 2.0 alongside elevated GGT is a classic alcohol pattern.
Medications
Many commonly used medications can raise liver enzymes as a side effect:
- Paracetamol — safe at recommended doses; causes severe ALT elevation in overdose
- Statins — mild transaminase elevation occurs in a small percentage of users; true liver injury is rare but warrants monitoring
- NSAIDs — ibuprofen and similar anti-inflammatories can cause hepatotoxicity with regular use
- Antibiotics — amoxicillin-clavulanate (Augmentin) is among the most common causes of drug-induced liver injury
- Anti-epileptics — carbamazepine, valproate, and others can elevate liver enzymes
- Herbal supplements — green tea extract, kava, and some bodybuilding products carry hepatotoxic risk
Always tell your GP about every supplement, herbal product, and over-the-counter medication you take when reviewing LFT results.
Metabolic syndrome and obesity
Insulin resistance, obesity, and metabolic syndrome are closely linked to fatty liver and elevated ALT. This is the most common cause of mildly elevated transaminases in Australian general practice.
Viral hepatitis
Hepatitis A, B, and C can all cause significant elevation of ALT and AST. Hepatitis B and C may be asymptomatic for years while quietly damaging the liver. In Australia, 230,000 people are estimated to be living with chronic hepatitis B (AIHW), and chronic hepatitis C affects approximately 117,000 Australians.
Muscle injury and exercise
AST is found in skeletal muscle as well as the liver. Intense exercise, particularly resistance training or endurance events, can transiently elevate AST. If AST is elevated but ALT is normal, muscle injury is a plausible explanation — creatine kinase (CK) testing can confirm.
Bone disease and growth
ALP is produced by bone cells during periods of increased bone turnover. Elevated ALP with normal GGT and normal bilirubin suggests a bone source — normal growth in adolescents, Paget's disease, fracture healing, or hyperparathyroidism.
Autoimmune conditions
Autoimmune hepatitis, primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC) can all produce abnormal LFTs. These conditions typically show specific patterns — elevated ALP and GGT in cholestatic diseases, elevated transaminases in autoimmune hepatitis — and are often accompanied by positive autoantibodies.
Thyroid dysfunction
Hypothyroidism can mildly elevate ALT and ALP. If LFTs are unexpectedly abnormal, checking TSH is worth considering.
When to discuss your results with your GP
Most mild LFT abnormalities are not cause for alarm, but there are circumstances where a conversation with your GP is warranted.
Consider discussing your results if:
- Any marker is more than twice the upper limit of the reference range
- Two or more markers are elevated at the same time, even mildly
- ALT or AST has been persistently elevated across two or more consecutive tests
- Bilirubin is elevated alongside ALP and GGT (cholestatic pattern)
- Albumin is low, particularly if other markers are also abnormal
- You have started a new medication and LFTs have worsened since
- You have metabolic risk factors (obesity, type 2 diabetes, high triglycerides) and want to understand your baseline
- You have a family history of liver disease or hereditary conditions like haemochromatosis
A single mildly elevated result with no associated symptoms often warrants repeat testing in 4–6 weeks before drawing conclusions. Many transient elevations resolve on their own — after illness, intense exercise, or a period of alcohol use — and do not indicate underlying disease.
The pattern across multiple tests over time is always more informative than a single result. This is one of the most valuable aspects of annual testing: establishing a personal baseline so that meaningful changes stand out.
How to support liver health through lifestyle
The liver has a remarkable capacity for recovery, particularly when modifiable drivers of liver stress are addressed early. The following lifestyle factors are consistently associated with liver health in clinical research — all framed as general information and not a substitute for advice from your GP.
Alcohol moderation
Alcohol is directly hepatotoxic. The Australian National Health and Medical Research Council (NHMRC) recommends no more than 10 standard drinks per week and no more than 4 on any single occasion to reduce long-term health risks. Regular alcohol use raises GGT and increases long-term risk of alcohol-related liver disease. Reducing alcohol intake is one of the most reliable ways to lower GGT and reduce liver burden.
Dietary pattern
A Mediterranean-style dietary pattern — emphasising vegetables, legumes, whole grains, olive oil, nuts, and fish while limiting refined carbohydrates, added sugars, and ultra-processed foods — is associated with reduced liver fat and lower ALT in multiple studies. Reducing sugar-sweetened beverages, particularly those high in fructose, is linked to lower liver fat accumulation.
Coffee consumption (regular or decaffeinated) is consistently associated with lower ALT and reduced liver disease risk in observational research.
Exercise and weight management
Regular exercise — both aerobic activity and resistance training — reduces liver fat and lowers ALT, even without significant weight loss. A reduction in body weight of 3–5% can reduce liver fat measurably; 7–10% weight loss can reduce liver inflammation and may help reverse early fibrosis in NAFLD. Any sustainable increase in physical activity is likely to be beneficial.
Medication and supplement awareness
Many people do not realise that some supplements and herbal products carry hepatotoxic risk. High-dose supplements — particularly green tea extract, kava, and certain traditional herbal formulations — have been associated with drug-induced liver injury. Reviewing all medications and supplements with your GP when LFTs are abnormal is essential.
Regular monitoring
For people with risk factors for liver disease — including metabolic syndrome, regular alcohol use, or a family history of liver conditions — annual LFT testing establishes a baseline and catches trends before they become clinical problems. Liver disease often progresses silently. Annual testing provides the data to have an earlier, more informed conversation with your GP.
Key Takeaways
- A liver function test (LFT) panel typically includes ALT, AST, GGT, ALP, albumin, total bilirubin, and total protein — each measuring a different aspect of liver health.
- Fatty liver disease affects more than 1 in 3 Australians and is the most common cause of mildly elevated ALT in general practice.
- Calculated ratios — De Ritis (AST:ALT), GGT:ALT, albumin-globulin, and bilirubin-to-albumin — add significant interpretive value beyond individual marker levels.
- A normal LFT result does not rule out fatty liver disease — up to 30% of people with confirmed fatty liver may have ALT within the standard reference range.
- Alcohol, medications, metabolic syndrome, viral hepatitis, and muscle injury are among the most common causes of abnormal LFT results in Australian adults.
- Tracking your LFT results annually establishes a personal baseline and makes meaningful trends visible before they become clinical problems.
- Always discuss persistently elevated, significantly abnormal, or pattern-based LFT results with your GP rather than interpreting them in isolation.
Frequently Asked Questions
AHPRA Disclaimer: This information is general in nature and should not replace individual medical advice. Always discuss your test results and health concerns with a registered healthcare practitioner.
References
- Gastroenterological Society of Australia (GESA). Patient Resources: Fatty Liver Disease. Melbourne: GESA, 2025.
- Coates P. Liver function tests. Australian Family Physician, 40(3):113–115, 2011.
- Australian Institute of Health and Welfare (AIHW). Liver Disease: Leading Cause of Premature Mortality in Australia (Fact Sheet). Canberra: AIHW, 2016.
- Kwo PY, Cohen SM, Lim JK. ACG Clinical Guideline: Evaluation of Abnormal Liver Chemistries. American Journal of Gastroenterology, 112(1):18–35, 2017.
- Rinella ME et al. AASLD Practice Guidance on the Clinical Assessment and Management of Nonalcoholic Fatty Liver Disease. Hepatology, 77(5):1797–1835, 2023.
- Younossi ZM, Corey KE, Lim JK. AGA Clinical Practice Update on Lifestyle Modification Using Diet and Exercise to Achieve Weight Loss in the Management of NAFLD. Gastroenterology, 160(3):912–918, 2021.
- Tan EX et al. Upper Limit of Normal ALT Levels in Health and Metabolic Diseases: Pooled Analysis of 423,355 Individuals. Alimentary Pharmacology and Therapeutics, 59(8):984–992, 2024.
- Valenti L et al. Definition of Healthy Ranges for Alanine Aminotransferase Levels: A 2021 Update. Hepatology Communications, 5(11):1824–1832, 2021.
- National Health and Medical Research Council (NHMRC). Australian Guidelines to Reduce Health Risks from Drinking Alcohol. Canberra: NHMRC, 2020.