When fatty liver is found in a lean person, measure waist circumference, blood pressure, blood glucose, HbA1c, triglycerides and HDL cholesterol. (File Photo)
Arun, a 44-year-old executive, walked into the clinic holding an ultrasound report with a mixture of confusion and disbelief. The scan, performed for recurrent acidity, had shown fatty liver. “But I am not fat,” he said. He had a point. His BMI (body mass index) was 22.6 kg/m², within the lean range for an Asian adult. He drank alcohol occasionally and his liver enzymes were mildly raised. By appearance, he seemed healthy.
But his waist measured 93 cm, triglycerides were elevated and HbA1c (average blood sugar count of three months) was in the prediabetes range. He had a desk job, ate generous portions of rice and refined cereals, exercised irregularly and had relatively little muscle. A fibrosis score based on routine blood tests was indeterminate. Liver elastography was therefore advised and showed greater stiffness than his appearance had suggested.
The diagnosis was lean metabolic dysfunction-associated steatotic liver disease (lean MASLD)—a reminder that thinness is not the same as metabolic health.
MASLD is the newer name for what was previously called non-alcoholic fatty liver disease. It refers to liver fat occurring alongside at least one cardiometabolic abnormality, such as high glucose, raised blood pressure, elevated triglycerides, low HDL cholesterol or excess adiposity. A person does not need to meet every criterion. Fatty liver accompanied by prediabetes or an increased waist circumference may be enough to place someone within the MASLD spectrum.
The definition of “lean” also varies with ethnicity. In Asian populations, lean MASLD generally refers to disease occurring at a BMI below 23 kg/m². This lower cut-off matters in India because South Asians often develop diabetes and other metabolic complications at a lower BMI than many Western populations. Arun was, therefore, not an exception. He belonged to a group that can easily be missed because fatty liver is commonly associated with excess body weight.
BMI measures weight relative to height but it does not show where fat is stored or how much muscle a person has. Two people with the same BMI can have very different metabolic profiles.
When the body’s capacity to store fat safely under the skin is exceeded, surplus fat can accumulate around abdominal organs and within the liver, pancreas and muscle. This visceral and ectopic fat triggers insulin resistance, inflammation and the release of fatty acids into the liver. A person may therefore have slim arms and legs while carrying metabolically harmful fat around the waist.
In South Asians, a waist circumference of 90 cm or more in men and 80 cm or more in women suggests central adiposity. A waist-to-height ratio of about 0.5 is another useful warning sign. The weighing scale may remain unchanged while the waist slowly expands.
Low muscle mass adds to the problem. Skeletal muscle is a major site for glucose disposal after meals. With less muscle, glucose may be cleared less efficiently, increasing metabolic stress on the liver. This “thin-fat” or sarcopenic phenotype becomes more important with ageing, inactivity, inadequate protein intake or repeated crash diets.
Fatty liver is sometimes treated as a harmless footnote on an ultrasound report. In some people it remains just that. In others, liver fat is accompanied by inflammation, called metabolic dysfunction-associated steatohepatitis (MASH). Over time, this can lead to fibrosis, cirrhosis and, in a smaller proportion, liver cancer. Lean patients can be diagnosed late because nobody expects them to have metabolic liver disease. Normal or near-normal liver enzymes do not reliably exclude significant fibrosis. Lean MASLD is associated with a higher risk of liver-related complications. Its cardiovascular risk compared with obesity-associated MASLD remains under study, but being lean does not protect against heart disease. Blood pressure, glucose, lipids, smoking and sleep apnoea still require attention. Arun’s report could not simply be dismissed with advice to “avoid oily food”.
When fatty liver is found in a lean person, measure waist circumference, blood pressure, blood glucose, HbA1c, triglycerides and HDL cholesterol. Alcohol intake and medicines should be reviewed. Other causes of liver fat or abnormal liver tests — including viral hepatitis and selected endocrine, autoimmune, nutritional and inherited conditions—should be considered according to the individual history and examination.
The next question is not merely, “Is there fat in the liver?” It is, “Has scarring begun?”
FIB-4 is a practical first assessment calculated from age, AST, ALT and platelet count. A value below 1.3 generally indicates a low probability of advanced fibrosis. Between 1.3 and 2.67, a second assessment, usually liver elastography, is recommended. A value above 2.67 warrants specialist evaluation. In adults over 65, a threshold of 2.0 is generally used to identify lower risk. For Arun, the indeterminate FIB-4 result was precisely why assessment did not stop with the ultrasound.
The usual advice to lose 7–10 per cent of body weight may be inappropriate for a lean person, particularly when muscle mass is already low. The aim is to reduce visceral fat, improve insulin sensitivity and preserve or build muscle. For an Indian diet, this often means reducing portions of polished rice, refined flour, sweets, fruit juice and sugar-sweetened drinks rather than eliminating carbohydrates altogether. Vegetables, pulses and appropriate protein sources should occupy more of the plate. Saturated fat and ultra-processed foods should be limited. Alcohol should be minimised or avoided depending on the clinical situation.
Exercise should include at least 150 minutes of aerobic activity each week along with resistance training on two or more days. Walking is valuable, but it is not a complete muscle-building programme. Strength training deserves to be part of the prescription.
Diabetes, prediabetes, hypertension and dyslipidaemia should be treated appropriately. Statins should not automatically be withheld because liver enzymes are mildly raised; cardiovascular protection remains important. Medicines should be individualised according to fibrosis stage, diabetes, lipid profile, nutritional status and the risk of further muscle loss.
Arun reduced refined-carbohydrate portions, added fibre-rich vegetables, pulses and protein, began supervised resistance exercise and received treatment for dyslipidemia. His weight changed little, but his waist, glucose control, strength and liver markers improved.
That is the central lesson of lean MASLD: measure what BMI misses.
(Dr Bhattacharya is senior endocrinologist at Apollo Hospital, Delhi)