Her blood test came back with one liver marker slightly raised. ALT, 48. The nurse rang to say it was nothing to worry about, probably the wine at Christmas, and they would repeat it in a year.
She is 54. She has not had a drink in six weeks. Her waist has grown three inches since her periods stopped, though the scales have barely shifted.
Nobody mentioned her liver again. Nobody connected it to her menopause either, and those two things are more closely related than almost any woman is told.
Fat accumulating in liver cells used to be called non-alcoholic fatty liver disease, or NAFLD. In 2023 it was renamed metabolic dysfunction-associated steatotic liver disease, MASLD, and the change was not cosmetic.
The old name defined the condition by what it was not. The new one names what it actually is: a liver problem driven by metabolic dysfunction, sitting alongside insulin resistance, visceral fat and raised triglycerides.
It affects roughly one in three adults worldwide, which makes it the most common chronic liver disease there is. Most people who have it do not know.
MASLD has always been more common in men. Before menopause, women are relatively protected.
Then that protection disappears.
In a study of 1,423 people, the prevalence of fatty liver was 27.2 per cent in postmenopausal women against 14.4 per cent in premenopausal women. Nearly double.
It is not a step change either. Incidence climbs steadily after menopause, peaks between 60 and 69, then falls again after 70.
And the comparison with men reverses entirely. Postmenopausal women are around 1.2 times more likely than men of the same age to develop fatty liver and to progress to serious fibrosis.
So the group at highest risk of a disease everyone associates with overweight middle-aged men is, in fact, women after menopause.
Three mechanisms, and they compound.
Fat moves inward. As oestrogen falls, fat redistributes from hips and thighs to the abdomen, including the visceral fat packed around your organs. That fat drains directly into the liver through the portal vein, delivering free fatty acids straight to it.
Receptors switch over. As oestrogen receptors in visceral fat cells are downregulated, androgen receptor expression rises. The tissue becomes more sensitive to androgens, which promotes further visceral accumulation. The loop feeds itself.
Insulin resistance develops. Visceral fat releases free fatty acids and inflammatory signals that impair insulin signalling. And insulin resistance drives liver fat accumulation directly, because insulin normally restrains fat production in the liver.
This is the same machinery behind the weight around your middle and the diabetes risk. Why weight gathers around your middle covers the fat side, and menopause and diabetes risk covers the glucose side. Your liver sits in the middle of both.
MASLD is famously silent. No pain, no symptoms, sometimes for decades.
When something does show, it is vague: tiredness, a dull ache under the right ribs, a sense of fullness. All easily attributed to menopause itself, which is exactly what happens.
And the blood test misleads. Liver enzymes are normal in a substantial proportion of people with MASLD, including some with significant fibrosis. A clean ALT does not rule it out.
The reverse is also true, and it is where women lose years. A mildly raised ALT in a woman of 54 gets attributed to alcohol, or to a virus, or to nothing at all. It rarely gets attributed to her metabolism, which is usually what it is.
If oestrogen deficiency drives this, replacing oestrogen should help. The picture is more interesting than that.
A South Korean cohort of 368 women tracked what happened over a year on hormone therapy, and the two routes did opposite things.
Oral HRT: MASLD prevalence rose from 25.3 to 29.4 per cent.
Transdermal HRT: prevalence fell from 24.0 to 17.3 per cent.
The difference between groups was statistically significant.
The likely explanation is first-pass metabolism. Oestrogen swallowed as a tablet goes straight to the liver in high concentration before reaching the rest of you, and it alters how the liver handles fats. Oestrogen absorbed through skin bypasses that entirely.
This is the same reason transdermal oestrogen carries a lower clot risk, and it is one more argument for the patch or gel if you have metabolic risk factors.
It is worth saying clearly: nobody prescribes HRT for your liver, the evidence base here is thin, and one cohort study is not a trial. But if you are choosing a route anyway, this belongs in the conversation. The truth about HRT research covers the wider picture.
Most women get liver enzymes and nothing else, which tells you almost nothing.
ALT and AST, with the understanding that normal does not exclude the condition.
A FIB-4 score. This is the useful one, and it is free. It uses your age, ALT, AST and platelet count, all of which appear on standard panels, to estimate how likely you are to have significant fibrosis. Any doctor can calculate it in seconds, and it is recommended as a first-line screen.
Liver ultrasound if fat is suspected. It detects steatosis but not the amount of scarring.
FibroScan if FIB-4 is intermediate or high. This measures liver stiffness and is far better at identifying fibrosis.
Alongside those: fasting glucose, fasting insulin, HbA1c, triglycerides and HDL. The liver rarely has a problem on its own, and our free insulin resistance calculator works out HOMA-IR from two of those numbers.
A reasonable sentence for an appointment: "My ALT was slightly raised and my waist has increased since menopause. Could we calculate a FIB-4 score?"
The genuinely good news is that liver fat responds faster than almost anything else in the body.
Losing 5 per cent of body weight reduces liver fat measurably. Ten per cent can improve inflammation and, in some people, early fibrosis. That is a smaller target than most women assume.
Resistance training reduces liver fat even without weight loss, because muscle takes up glucose that would otherwise be converted to fat in the liver.
Cutting fructose, particularly from sugary drinks, matters more than for most conditions. Fructose is processed almost entirely by the liver and converted to fat more readily than glucose.
Coffee, unexpectedly, is one of the better-evidenced dietary factors. Regular consumption is associated with less fibrosis progression in people who already have MASLD.
Alcohol, even at levels well within guidelines. A liver already handling metabolic stress has less capacity for anything else. Alcohol and women's hormones covers the wider picture.
And if you are on a GLP-1 medication, that is relevant here too. These drugs are being actively studied for MASLD, and the weight loss alone reduces liver fat substantially.
Because most people with MASLD do not die of liver disease.
They die of cardiovascular disease, and MASLD is an independent marker of that risk. It is your liver telling you something about your whole metabolism, and it does so before your heart does.
Which makes a slightly raised ALT in a woman of 54 worth a second look, rather than a repeat test in a year.
What is MASLD?
Metabolic dysfunction-associated steatotic liver disease, previously called NAFLD. Fat accumulating in liver cells alongside metabolic problems such as insulin resistance and visceral fat. It affects roughly one in three adults.
Why does menopause increase the risk?
Falling oestrogen shifts fat to the abdomen, where it drains directly into the liver. Oestrogen receptors in fat cells are downregulated while androgen receptors rise, promoting further visceral accumulation, and insulin resistance develops alongside.
How much does risk actually rise?
One study found fatty liver in 27.2 per cent of postmenopausal women against 14.4 per cent of premenopausal women. Postmenopausal women are also around 1.2 times more likely than men of the same age to develop it and progress to serious fibrosis.
Can I have it with normal liver enzymes?
Yes. Liver enzymes are normal in a substantial proportion of people with MASLD, including some with significant fibrosis. A FIB-4 score is more informative and costs nothing to calculate.
Does HRT help or harm?
The route appears to matter. In one cohort, oral HRT was associated with prevalence rising from 25.3 to 29.4 per cent over a year, while transdermal fell from 24.0 to 17.3 per cent. Likely explained by first-pass liver metabolism. This is not a reason to start or stop HRT, but it is worth raising when choosing a route.
Is it reversible?
Early MASLD responds well. Losing 5 per cent of body weight measurably reduces liver fat; 10 per cent can improve inflammation and sometimes early fibrosis. Resistance training reduces liver fat even without weight loss.
What should I ask my doctor for?
A FIB-4 score from your existing bloods, plus fasting glucose, insulin and triglycerides. An ultrasound if fat is suspected, and a FibroScan if FIB-4 is intermediate or high.
Sources: Milani I, Chinucci M, Leonetti F, Capoccia D, MASLD: prevalence, mechanisms, and sex-based therapies in postmenopausal women, Biomedicines 2025;13(4):855 · Sullivan J, Harris D, Moreno LE, Menopause and increased risk of metabolic dysfunction-associated steatotic liver disease, Am Fam Physician 2026 · Ryu S et al., The influence of metabolic factors for nonalcoholic fatty liver disease in women, Biomed Res Int 2015 · The impact of estrogen deficiency on liver metabolism: implications for hormone replacement therapy, 2026 · Educational only, not medical advice. Raised liver enzymes should be assessed by a doctor.
Keep reading: Menopause and diabetes risk · Why weight gathers around your middle · The truth about HRT research · Alcohol and women's hormones · Waist-to-height ratio · Take the free Hormone Quiz