A normal weight does not guarantee protection from fatty liver disease. Fat can build up in the livers of lean people because of increased visceral fat around the organs, insulin resistance or impaired fat metabolism. The disease may remain without clear symptoms for a long time, while assessing its risks requires looking at waist circumference, muscle mass, and blood sugar and fat levels, rather than only the figure shown on the scales.
The new name for the disease and its link to metabolic dysfunction
Under the modern classification in European guidelines, the disease is known as metabolic dysfunction-associated steatotic liver disease, abbreviated as MASLD, when fat accumulation in the liver occurs alongside one or more cardiometabolic risk factors.
This name replaced the term non-alcoholic fatty liver disease, commonly abbreviated as NAFLD, in the latest classification of the disease. Dr Marie-Noelle Class Chammal, a specialist in endocrinology, diabetes and obesity at Bellevue Medical Centre in Beirut, said fatty liver cases among lean people account for about 10 to 20% of all cases.
Waist circumference reveals hidden visceral fat
She explained that the problem is not linked to body weight alone, but also to where fat accumulates and how efficiently metabolic processes work. This means it can affect people whose weight appears normal. Chammal added that people with a normal weight but an increased waist circumference are among those at greatest risk, as this may indicate accumulated visceral fat around the internal organs.
Two people may weigh the same, but have different fat distributions and body compositions, making metabolic and liver risks higher for one of them despite similar figures on the scales. The likelihood of the disease also rises among people with insulin resistance or prediabetes, and among those who have both high triglycerides and low levels of good cholesterol.
Women with polycystic ovary syndrome are also among the groups at risk, because it is associated with metabolic disorders that may affect how the body handles sugar and fat. Other risk factors include uncontrolled hypothyroidism and reduced muscle mass, particularly among older people.
Genetic predisposition may play a role in some people, including variants in the PNPLA3 gene. Risk is also associated with excessive consumption of sugars, sweetened drinks and ultra-processed foods, even when this dietary pattern does not result in visible obesity.
A review by experts from the American Gastroenterological Association, published in the journal Gastroenterology, estimated that lean people account for between 7 and 20% of those with non-alcoholic fatty liver disease. The review recommended assessing type 2 diabetes, lipid disorders and high blood pressure in this group, rather than ruling out the possibility of disease on the basis of normal weight.
Waist-to-height ratio identifies risk
Measuring waist circumference is a practical way to obtain information that weight alone does not reveal, according to Chammal, who pointed to a simple rule of trying to keep waist circumference below half a person’s height. Comparing the two measurements helps identify central fat that may be present in someone who is not classified as overweight or obese.
When do indicators warrant a liver health assessment?2es1
Chammal advised considering a liver health assessment in the presence of diabetes or prediabetes, repeatedly elevated liver enzymes, or steatosis discovered by chance during an imaging examination. Other reasons include an increased waist circumference or a family history of diabetes or cirrhosis, even when a person’s weight is within the normal range.
These indicators do not mean that all lean people need routine screening for fatty liver. The American Gastroenterological Association does not recommend screening every lean person, but instead calls for a focus on risk factors and metabolic disorders. Once the disease is confirmed, priority shifts to estimating the likelihood of fibrosis and whether the patient needs additional follow-up.
Chammal explained that assessing a patient involves more than measuring liver enzymes. It also includes ruling out other possible causes of fat accumulation or liver damage on the basis of the medical history. These causes include alcohol consumption, viral hepatitis, some autoimmune diseases, and medicines that may affect the liver or contribute to fat accumulation in it.
Metabolic assessment may include fasting blood sugar, glycated haemoglobin, a lipid profile and thyroid function tests. Depending on each patient’s condition, a doctor may request an oral glucose tolerance test or an assessment of insulin resistance. Chammal also stressed the importance of measuring waist circumference and analysing body composition to assess visceral fat and muscle mass more accurately.
After fat is detected in the liver, the most important step is to determine the likelihood of fibrosis. The 2024 European guidelines recommend a stepwise assessment pathway that begins with non-invasive blood-based scores, including the FIB-4 index, before moving to liver stiffness measurement techniques when initial results indicate that this is necessary.
Chammal stressed that treating a lean patient should not become a race to reduce the number shown on the scales. The main goal is to improve body composition by reducing visceral fat while maintaining or increasing muscle mass. Poorly planned weight loss may lead to muscle loss, which does not achieve the required therapeutic objective in this group.
She recommended resistance training two to 3 times a week, alongside about 150 to 200 minutes of aerobic activity each week. She also called for limiting sweetened drinks and ultra-processed foods, and adopting a Mediterranean-style diet that provides an appropriate amount of protein, helping to protect muscle while reducing harmful fat.
Some patients may benefit from limited weight loss of about 3 to 5% of their body weight, provided it does not come at the expense of muscle mass. Other important measures include improving sleep and treating sleep apnoea when present, because addressing associated factors is part of improving the patient’s overall metabolic health.
European guidelines recommend that people of normal weight with metabolic dysfunction-associated steatotic liver disease follow a healthy diet and engage in physical activity to reduce the amount of fat in the liver. The guidelines are based on a year-long trial in which weight loss of between 3 and 5% restored liver fat to normal levels in about half of the participants who did not have obesity.
Chammal said insulin resistance may be a main driver of the disease even in lean people. Controlling diabetes, lipids and insulin resistance is therefore not separate from treating the liver problem, but part of protecting it. Managing the condition requires addressing the metabolic dysfunction that contributes to the continued accumulation of fat in the liver and the worsening of its risks.
Some diabetes medicines may provide metabolic and liver benefits for selected patients, but Chammal stressed that the choice of medicine should be based on the patient’s condition and made under medical supervision. These safeguards are particularly important for people of normal weight, because weight loss may not be an appropriate treatment goal for them even when they need to improve their metabolic indicators.
Regarding statins used to lower cholesterol, Chammal said they are generally safe for people with fatty liver when prescribed for a medical need. She warned against stopping them without consulting a doctor because of a slight rise in liver enzymes. Guidelines from the American Association for the Study of Liver Diseases confirm that statins can be used when necessary to reduce the risks of cardiovascular disease.
Dr Mustafa Addous, a general practitioner at a medical centre in Qatar, said normal weight does not constitute a «clean bill of health» against lipid disorders. He explained that some lean people may develop fatty liver because of deep fat accumulating around the viscera, alongside insulin resistance and impaired fat metabolism, even though their outward appearance does not suggest a problem.
Addous said the disease may remain silent for a long time because there are no clear early symptoms, and some patients may feel nothing more than mild fatigue. It is therefore often discovered by chance, either after elevated liver enzymes appear in blood tests or during an ultrasound examination, known as a sonogram, performed for another reason.
Non-invasive methods can now assess liver damage and the possible degree of fibrosis. These include FibroScan, which measures liver stiffness and helps the doctor estimate the likelihood of fibrosis. He stressed that preventing and reducing fat accumulation depend largely on movement and exercise, cutting down on sugar and fizzy drinks, and improving lifestyle even among people whose weight appears ideal.
Developing the disease while lean does not mean it is less serious. A 2024 meta-analysis published in the journal Annals of Hepatology, covering 14 studies involving 94,181 people with fatty liver, found that lean people accounted for 11.3% of the affected participants, confirming that the disease is present in this group at a rate that cannot be ignored.
After a median follow-up period of 8.4 years, the researchers found that fatty liver in lean people was associated with an approximately 1.6-fold increase in the risk of death from all causes compared with affected people who were not lean. At the same time, the researchers said that explaining the causes of this complex relationship still requires further studies.
The scales alone therefore do not provide a complete picture of liver health. Weight may remain normal while fat accumulates in internal locations that carry greater risks. Waist circumference, blood sugar, lipids, muscle mass and family history can help identify the risk, while early diagnosis allows dietary changes, increased activity, control of metabolic disorders, and assessment and monitoring of fibrosis.
