Fatty liver: one in three Australians have it, and a normal blood test won't rule it out.

MASLD, metabolic dysfunction-associated steatotic liver disease, renamed from NAFLD by international consensus in 2023, is excess fat stored inside liver cells in someone who also carries at least one cardiometabolic risk factor. It is the most common liver disease in Australia and, on the best national data available, affects roughly one in three adults. Almost all of them feel completely well. And here is the part that matters most for anyone who has ever been told their liver tests were "fine": in that same Australian cohort, only 13% of adults had an elevated ALT. A normal liver function test is not a clean bill of liver health.

The key facts, up front

• 37% of Australian adults had fatty liver disease in the nationwide AusDiab study of 4,747 adults, but only 22% of those with fatty liver had a raised ALT. The disease is largely invisible to routine testing.
• Fibrosis is the only feature that predicts death. Not the amount of fat, not the inflammation score. Two independent long-term biopsy cohorts converged on this, one of them following patients for up to 33 years.
• You can calculate your own fibrosis risk for free. FIB-4 uses age, AST, ALT and platelet count. Four numbers already sitting on most standard blood panels, almost never combined into a score.
• It is reversible. 10% body weight loss produced resolution of steatohepatitis in 90% of patients and fibrosis regression in 45% in the largest lifestyle-intervention biopsy study to date.
• It is not primarily a liver problem. The leading cause of death in people with MASLD is cardiovascular disease, not liver failure, which is why it belongs in a preventative health workup rather than a gastroenterology silo.

Why the name changed: and why that matters

In 2023, a Delphi consensus of 236 panellists from 56 countries convened by the AASLD, EASL and ALEH retired the term "non-alcoholic fatty liver disease". Two-thirds of respondents considered the word "fatty" stigmatising, and 61% said the same of "non-alcoholic". More substantively, defining a disease by what it isn't obscured what it is: a hepatic manifestation of metabolic dysfunction. The new name, MASLD, requires at least one cardiometabolic criterion, raised waist circumference, elevated glucose or type 2 diabetes, raised blood pressure, high triglycerides, or low HDL.

That reframing is clinically useful. It tells you where to look. If you have fat in your liver, the same process is almost certainly affecting your fasting insulin, your triglycerides and your cardiovascular risk, and the liver finding is often the earliest visible signal of the cluster.

What the clinical evidence actually shows

• AusDiab, the Australian benchmark (Farrell et al. Scientific Reports 2022): in 4,747 Australian adults aged 34–97, 37% met criteria for metabolic-associated fatty liver disease. Elevated ALT was present in just 13% of the total cohort. Of those with fatty liver, 61% had a BARD score suggesting risk of advanced fibrosis. This is the most directly relevant prevalence data we have for Australia, and it is the origin of the "you can have this with normal bloods" problem.
• Fibrosis, not inflammation, predicts outcomes (Angulo et al. Gastroenterology 2015): across a large multinational biopsy cohort, liver fibrosis, and no other histological feature, was associated with long-term mortality and liver transplantation. The NAFLD activity score, which grades fat and inflammation, did not independently predict death.
• Confirmed over 33 years (Ekstedt et al. Hepatology 2015): in a Swedish cohort followed for up to three decades, fibrosis stage was the strongest predictor of disease-specific mortality. Patients at fibrosis stage 3–4 had roughly three times the mortality risk regardless of their activity score.
• Weight loss reverses it (Vilar-Gomez et al. Gastroenterology 2015): in 261 patients with paired biopsies after a year of lifestyle intervention, those achieving ≥10% weight loss had 90% resolution of steatohepatitis and 45% fibrosis regression. Under 5% weight loss produced resolution in about 10%. The relationship is steeply dose-dependent, which is an argument for aiming high rather than settling for "a few kilos".
• GGT is a cardiovascular marker too (Ruttmann et al. Circulation 2005): in 163,944 Austrian adults followed up to 17 years, GGT independently predicted cardiovascular mortality. Adjusted hazard ratio approximately 1.66 in men and 1.64 in women per log increase, with a clear dose-response. A creeping GGT is not just a question about your wine intake.
• Drug therapy has finally arrived (Harrison et al. NEJM 2024; Sanyal, Newsome et al. NEJM 2025): in the phase 3 MAESTRO-NASH trial, resmetirom achieved steatohepatitis resolution in 26–30% of patients versus 9.7% on placebo, and fibrosis improvement in 24–25% versus 14.2%. The phase 3 ESSENCE trial of semaglutide 2.4 mg in 1,197 patients likewise met both endpoints at 72 weeks. Notably, placebo response rates of 10–14% are high. A reminder that trial-level effect sizes are modest and these are additions to, not replacements for, metabolic treatment.

FIB-4: the fibrosis score hiding in your existing blood test

Almost every standard blood panel already contains the four inputs. FIB-4 combines them:

It was originally developed by Sterling and colleagues in 2006 for HIV/HCV co-infection, where a cut-off below 1.45 excluded advanced fibrosis with a 90% negative predictive value. The 2023 AASLD practice guidance adopted it as the first-line risk-stratification step for fatty liver disease, with these thresholds for adults aged 35–65:

• Below 1.3, advanced fibrosis unlikely. Reassess periodically; the metabolic drivers still need attention.
• 1.3 to 2.67, indeterminate. The honest label. This zone warrants a second-tier test, usually transient elastography (FibroScan).
• Above 2.67, high risk. Specialist hepatology assessment is indicated.
• Over age 65. Use 2.0 as the lower threshold, because FIB-4 contains age in the numerator and drifts upward regardless of liver health.

Be clear about its limits, because this is where honest medicine matters: FIB-4 was not derived in a MASLD population, it performs poorly under age 35, and the indeterminate band is uncomfortably wide. It is a triage tool, not a diagnosis. What it does well is the thing that matters most at population scale. Cheaply identifying the minority who need imaging, from the majority who don't.

How HodieLabs interprets your liver markers

Every biomarker in the HodieLabs Evidence-Based Clinical Library is interpreted against published clinical authority standards, not arbitrary "optimal" ranges. For the liver cluster:

• ALT. Healthy upper limit under 30 U/L (male) / under 19 U/L (female). These updated thresholds are substantially tighter than the reference intervals most Australian labs flag against, which were derived from populations that already included large numbers of people with undiagnosed fatty liver. An ALT of 38 U/L is commonly reported as normal and is, in a lean healthy adult, not.
• GGT, under 60 U/L (male) / under 38 U/L (female) on Australian RCPA reference intervals. Sensitive to alcohol, but also to oxidative stress, medications and metabolic syndrome, and independently predictive of cardiovascular mortality.
• AST/ALT ratio. 0.8 to 1.3 in healthy adults. In metabolic fatty liver the ratio typically sits below 0.8 until fibrosis develops; a ratio rising above 1 over serial tests is a meaningful trend signal. Above 2.0 points toward advanced fibrosis or alcohol-related liver injury.
• Platelets, a falling platelet count in someone with metabolic risk factors is an underappreciated early marker of portal hypertension, and is the input that does most of the work in a rising FIB-4.

Interpreted individually, each of these can look unremarkable. Interpreted together, and tracked over time, they form a pattern, which is the entire argument for reading biomarkers as a system rather than a checklist.

What the evidence does not say

Being honest about the limits is part of the point. Population screening for MASLD in unselected adults is not currently recommended by any major guideline body. The evidence that screening everyone improves outcomes doesn't yet exist. Most people with fatty liver will never develop cirrhosis. No supplement, not milk thistle, not vitamin E outside specific biopsy-proven cases, not any of the "liver detox" category, has evidence approaching that of weight loss and exercise. And a single FIB-4 in the indeterminate range is not a diagnosis of anything; it is a prompt to look further.

What the evidence does support is targeted assessment in people who carry metabolic risk factors, and acting decisively on the fibrosis signal when it appears.

The Australian gap

Liver function tests are among the most frequently ordered blood tests in Australian general practice, and are usually read as a binary: flagged, or not flagged. The result is a system that orders the right inputs and then discards most of the information in them. Four numbers that could be combined into a validated fibrosis score sit unlinked on the same page. A 2025 Medical Journal of Australia consensus statement on assessing metabolic dysfunction-associated fatty liver disease in primary care exists precisely because this gap is now recognised, but translating it into routine practice is unfinished work.

How testing works at HodieLabs

ALT, AST, GGT, ALP, bilirubin, albumin and platelets are measured in every Health Blueprint at our Melbourne Preventative Health & Longevity Clinic, alongside the full metabolic panel, fasting insulin, HbA1c, triglycerides and body composition. Your liver markers are interpreted against the standards above, combined into a FIB-4 score, and read in the context of the metabolic drivers behind them. Where the score or the trend indicates it, FibroScan or hepatology referral is arranged. Where it doesn't, the work is on the metabolic cause.

The bottom line

MASLD is common, largely silent, and mostly benign. Except in the minority where fibrosis is quietly accumulating, and in whom it is one of the more reversible serious conditions in medicine. The distinction between those two groups is not made by a "normal" liver function test. It is made by combining the numbers you already have, reading them against evidence-based thresholds rather than lab flags, and treating the metabolic dysfunction underneath.

References

1. Rinella ME, Lazarus JV, Ratziu V, et al. A multisociety Delphi consensus statement on new fatty liver disease nomenclature. J Hepatol. 2023;79(6):1542–1556.
2. Farrell AM, Magliano DJ, Shaw JE, et al. A problem of proportions: estimates of metabolic associated fatty liver disease and liver fibrosis in Australian adults in the nationwide 2012 AusDiab Study. Sci Rep. 2022;12(1):1956.
3. Angulo P, Kleiner DE, Dam-Larsen S, et al. Liver fibrosis, but no other histologic features, is associated with long-term outcomes of patients with nonalcoholic fatty liver disease. Gastroenterology. 2015;149(2):389–397.
4. Ekstedt M, Hagström H, Nasr P, et al. Fibrosis stage is the strongest predictor for disease-specific mortality in NAFLD after up to 33 years of follow-up. Hepatology. 2015;61(5):1547–1554.
5. Sterling RK, Lissen E, Clumeck N, et al. Development of a simple noninvasive index to predict significant fibrosis in patients with HIV/HCV coinfection. Hepatology. 2006;43(6):1317–1325.
6. Rinella ME, Neuschwander-Tetri BA, Siddiqui MS, et al. AASLD Practice Guidance on the clinical assessment and management of nonalcoholic fatty liver disease. Hepatology. 2023;77(5):1797–1835.
7. Ruttmann E, Brant LJ, Concin H, et al. Gamma-glutamyltransferase as a risk factor for cardiovascular disease mortality: an epidemiological investigation in a cohort of 163,944 Austrian adults. Circulation. 2005;112(14):2130–2137.
8. Vilar-Gomez E, Martinez-Perez Y, Calzadilla-Bertot L, et al. Weight loss through lifestyle modification significantly reduces features of nonalcoholic steatohepatitis. Gastroenterology. 2015;149(2):367–378.
9. Harrison SA, Bedossa P, Guy CD, et al. A phase 3, randomized, controlled trial of resmetirom in NASH with liver fibrosis. N Engl J Med. 2024;390(6):497–509.
10. Sanyal AJ, Newsome PN, Kliers I, et al. Phase 3 trial of semaglutide in metabolic dysfunction-associated steatohepatitis. N Engl J Med. 2025.
11. Younossi ZM, Koenig AB, Abdelatif D, et al. Global epidemiology of nonalcoholic fatty liver disease. Meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology. 2016;64(1):73–84.
12. Assessment of metabolic dysfunction-associated fatty liver disease in primary care: a consensus statement summary. Med J Aust. 2025;223(5).

This article is general information, not medical advice. Speak with your GP about what testing and care is appropriate for you.