Fatty liver disease: MAFLD diagnosis, fibrosis risk, cardiovascular focus, and menopause
A GP-facing summary of Professor Simone Strasser’s fatty liver presentation — positive diagnosis, FIB-4 / FibroScan stratification, why non-cirrhotic patients die of heart disease and cancer, and practical lifestyle plus drug messaging.
- Speaker
- Professor Simone Strasser — hepatologist, Royal Prince Alfred Hospital, Sydney; past president, Gastroenterological Society of Australia; major clinical and research interests in viral hepatitis, advanced liver disease, and clinical trials (fatty liver, viral hepatitis, liver cancer). Named in the preceding lecture outro; recording played in her absence.
Key messages
- We can make a positive diagnosis of metabolic dysfunction–associated fatty liver disease (MAFLD) — it is no longer only a diagnosis of exclusion.
- Postmenopausal women are at particular risk of MAFLD and of progressive liver disease.
- Risk-stratify everyone with fatty liver for hepatic fibrosis (FIB-4 ± FibroScan / blood fibrosis markers).
- Manage cardiovascular risk in all — CVD is the leading cause of death in many with non-cirrhotic disease.
- Identify who needs liver specialist review — roughly one in three adult Australians has this condition; specialists cannot see everyone.
Case: Anne — “just a bit of fatty liver”
Anne is 55, married with two adult children, sedentary medical secretary work, non-smoker, minimal alcohol. Persistent mildly abnormal liver enzymes for ~10 years; prior ultrasound showed diffuse fatty infiltration and she was told not to worry — “just a bit of fatty liver.”
Comorbidities: hypertension, dyslipidaemia, type 2 diabetes for five years (A1c 7.8% — undertreated), osteoarthritis, GORD, BMI 32, mild depression, early menopause at 44. Nothing targeted for weight loss. The seminar reframes: fatty liver plus metabolic disease is an opportunity for proactive cardiometabolic and fibrosis care — not reassurance alone.
NAFLD → MAFLD → MASLD (terminology)
“Non-alcoholic fatty liver disease” (NAFLD) was awkward: alcohol and metabolic disease can coexist, and “non-alcoholic” defined the condition by what it was not. In 2020, Professor Jacob George and Mel Eslam (Westmead) led an international consortium toward MAFLD — a positive diagnosis when there is steatosis (or high likelihood) plus metabolic criteria.
Fatty liver on imaging (or equivalent) plus overweight/obesity (ethnicity-adjusted) or type 2 diabetes — even if another liver disease coexists (e.g. alcohol-related disease, viral hepatitis, PBC). Severe obesity + type 2 diabetes was framed as >90% chance of fatty liver. Lean MAFLD: normal/low BMI but ≥2 metabolic risk abnormalities (often high waist circumference, hypertension, dyslipidaemia) — seen in younger people and some ethnicities with genetic predisposition (e.g. PNPLA3 variant discussed).
Europe/North America later preferred MASLD (metabolic dysfunction–associated steatotic liver disease) because “fatty” was seen as stigmatising; that literature path also keeps alcohol-exclusion thresholds closer to old NAFLD and defines MetALD / alcohol-related categories by alcohol grams/day. Australian guidance to GPs (as presented) often keeps the MAFLD-style frame so metabolic and alcohol drivers can be managed in parallel.
Inflammatory progressive form: MASH (metabolic dysfunction–associated steatohepatitis) — analogous to older NASH terminology for literature extrapolation.
How common — and menopause risk
- ~1 in 3 Australians living with MAFLD.
- With type 2 diabetes: ~2 in 3; obesity up to ~70%; hypertension alone ~50%; overt metabolic syndrome ~70% (figures as presented).
- Rising in adolescents with obesity, sedentary behaviour, and ultra-processed diets — advanced disease and liver cancer emerging by mid-adulthood after decades of steatosis.
MAFLD incidence is overall higher in men (~1.6-fold), but in women incidence rises especially from age ~50. Premenopausal oestrogens appear protective; early/abrupt loss of endogenous oestrogen (early menopause <50) associates with higher MAFLD, steatohepatitis, prediabetes, dyslipidaemia, progressive liver disease, and CV risk. Postmenopausal incidence was framed ~2.37-fold higher than premenopausal. Menopause shifts adiposity pattern, hepatic insulin sensitivity, and muscle — amplifying metabolic risk.
A large Korean cohort (~171,000) was cited linking depression and fatty liver, strongest as an independent factor in premenopausal women — worth noting alongside other metabolic risks.
~30% of liver cancers driven by fatty liver now occur without cirrhosis — screening pathways for that group remain uncertain; cirrhosis still warrants HCC surveillance as usual.
Why worry: CV death, cancer, and liver outcomes
For hepatologists: cirrhosis, liver failure, HCC, transplant — MAFLD/metabolic risk is a major driver and a cofactor in other liver diseases. For GPs: non-cirrhotic MAFLD patients are more likely to die of cardiovascular disease or (non-liver) cancer than of liver disease. Only a minority with simple steatosis have future liver events (~5% framed); as fibrosis rises (F2–F4), liver events rise — yet ~a quarter may still die of CV events, and obesity-related cancers remain relevant.
MAFLD can predate diabetes and other cardiometabolic diagnoses by ≥10 years. Fat on an ultrasound years ago was never “just fatty liver” — it was an early metabolic warning. Missed case-finding leads to surprise cirrhosis or HCC presentations.
FIB-4, FibroScan, and who to refer
An MJ-published algorithm (integrated into HealthPathways nationally, as stated) for primary care:
| Step | Action |
|---|---|
| 1 | Confirm steatosis / MAFLD context |
| 2 | Calculate FIB-4 (age, AST, ALT, platelets) — Liver Foundation calculator cited (liver.org.au) |
| < 1.3 | Advanced fibrosis unlikely — focus on cardiometabolic care |
| 1.3–2.67 | Indeterminate — second-line FibroScan (or ELF / Hepascore if accessible; not always Medicare-funded) |
| > 2.67 | Advanced fibrosis likely — specialist pathway |
FibroScan (vibration-controlled transient elastography): ~5 minutes in liver clinics; better validated than many shear-wave approaches (as presented). Liver stiffness <1.3 excludes advanced fibrosis well (high NPV); >2.67 suggests advanced fibrosis. CAP score quantifies fat — motivating for weight-loss goals and independently linked to outcomes. Serial FibroScan can track progression without biopsy for many patients.
In cirrhosis, poorly controlled diabetes was framed as ~14-fold higher risk of decompensation; hypertension drives fibrosis progression; stacking multiple metabolic risks (diabetes, age, hypertension, prior CV event) similarly escalates liver decompensation risk. Optimise diabetes and BP for liver and heart outcomes.
Do not refer every abnormal LFT or ultrasound fatty liver without FIB-4 first. Refer those with significant fibrosis risk or complex disease.
Lifestyle, Mediterranean diet, coffee, drugs
Multidisciplinary care starts in primary care: lifestyle, weight, diabetes optimisation; add dietitians/endocrinology/gastroenterology as needed. Menopause is a major driver with unmet research needs.
- Lifestyle is the cornerstone — often more sustainable than GLP-1 therapy unless long-term adherence is planned.
- Change eating patterns; reduce alcohol (sometimes to zero); increase physical activity.
- Coffee — framed as beneficial; 3–5 cups/day better than one (not sugar-laden “Pokémon” café drinks — Otter misheard; intent was sugary coffee drinks).
- Liver Foundation fatty liver / Mediterranean-style diet resources adapted across cultures; handout cards mentioned.
- Actively manage obesity (pharmacotherapy, bariatric surgery where appropriate), type 2 diabetes, lipids, hypertension.
- Statins are safe in fatty liver disease — improve liver tests, reduce CV mortality (what many die from), and were framed as reducing all-cause death and liver-related events. Do not withhold solely because of MAFLD.
- SGLT2 inhibitors — emerging liver benefit (phase 2 / observational evidence as presented).
- GLP-1 receptor agonists — important; Wegovy-dose for NASH/MASH not currently approved in Australia at the time of the talk, but expected soon for MAFLD use.
Back to Anne: target weight, diabetes, lipids, BP, lifestyle, fibrosis triage — the “don’t worry” message is outdated.