Fatty Liver Disease (MASLD): Causes, Symptoms, and When to See a Specialist

By Dr. Chetan Kalal | Hepatologist & Liver Transplant Physician, Gleneagles Hospital, Mumbai
Medically reviewed and updated: June 2026

Key Takeaways

• MASLD is the new medical name for what is commonly called “fatty liver” — replacing NAFLD in 2023
• 1.3 billion people globally have MASLD; projections reach 1.8 billion by 2050
• Indians are at disproportionate risk due to lower BMI thresholds, high diabetes prevalence, and dietary patterns
• You can have MASLD at a normal body weight — “lean fatty liver” affects up to 15% of MASLD patients
• In early and intermediate stages, the condition is reversible with the right intervention
• MASH-related cirrhosis is now the fastest-rising reason for liver transplant worldwide — most cases were preventable
• FibroScan is the best non-invasive way to know exactly where you stand — symptoms alone are unreliable

What Is MASLD? The Name Your Doctor Uses Today

If you have been told you have “fatty liver,” your doctor may now use a different term: MASLD, which stands for Metabolic Dysfunction-Associated Steatotic Liver Disease.

This is not a new disease. It is the same condition previously called Non-Alcoholic Fatty Liver Disease (NAFLD). In 2023, a global consortium of liver disease experts retired the old name after concluding it was misleading — “non-alcoholic” defined the disease by what it wasn’t, and “fatty” carried unnecessary stigma. The new name, MASLD, correctly names what is actually happening: fat accumulates in the liver as a direct consequence of underlying metabolic dysfunction — insulin resistance, high blood sugar, elevated triglycerides, high blood pressure, and excess body fat.

To meet the criteria for MASLD, a patient must have liver steatosis (fat on imaging or biopsy) plus at least one of five cardiometabolic risk factors:

1. Elevated BMI or waist circumference
2. Elevated fasting blood glucose or HbA1c
3. Elevated blood pressure
4. Elevated triglycerides
5. Low HDL cholesterol

For South Asians — including Indians — the BMI threshold is lower: ≥23 kg/m², not the Western standard of ≥25 kg/m². This matters enormously. Many Indian patients are dismissed because they appear slim, when their metabolic profile already places them firmly within MASLD criteria.

The spectrum of disease runs from simple steatosis (fat alone, largely benign) through MASH (Metabolic dysfunction-Associated SteatoHepatitis — fat plus inflammation and liver cell damage), to fibrosis, cirrhosis, and liver cancer.

How Common Is It — And Why India Is a High-Risk Country

The scale of this disease is difficult to overstate. According to a landmark 2026 analysis published in The Lancet Gastroenterology & Hepatology using Global Burden of Disease data, approximately 1.3 billion people — 16.1% of the world’s population — were living with MASLD in 2023. That number is projected to reach 1.8 billion by 2050, a 42% increase driven primarily by population growth in South Asia and North Africa.

India sits at the epicentre of this epidemic for reasons that go beyond simple obesity:

• The diabetes connection. India has over 100 million people with type 2 diabetes. The relationship between diabetes and MASLD is bidirectional — each worsens the other. Studies consistently show that 70–80% of patients with type 2 diabetes have MASLD on imaging.
• Visceral adiposity at lower body weight. Indians accumulate more fat around internal organs — including the liver — at lower BMIs than Western populations. A person at 24 kg/m² in India carries a metabolic risk equivalent to someone at 28–30 kg/m² elsewhere.
• Diet. High consumption of refined carbohydrates (maida, white rice, sugary beverages, processed snacks) drives hepatic fat accumulation independent of total caloric intake. The traditional Indian diet, when urbanised and processed, becomes a near-perfect substrate for metabolic liver disease.
• Physical inactivity. Desk-bound urban working patterns have created a generation of metabolically unhealthy Indians who appear outwardly “normal.”

The NRI dimension compounds this. Indians living in the UK, USA, Canada, and the Gulf — often eating hybrid diets, sitting long hours, managing stress — carry the same South Asian metabolic predisposition but frequently access specialist liver care only when symptoms are advanced, or when they return to India for a comprehensive workup.

The Lean Fatty Liver: A Warning Specifically for Indians

One of the most dangerous misconceptions about fatty liver is that it only affects people who are overweight. It does not.

Up to 10–15% of all MASLD patients are lean — defined as BMI below 25 kg/m² in Western populations, and below 23 kg/m² in Asians. In clinical practice in India, I see lean MASLD regularly: slender, physically active individuals with mildly elevated liver enzymes, incidental fatty liver on ultrasound, and no suspicion of liver disease until a routine health check forces the issue.

Lean MASLD is not benign. Research shows that lean patients with MASLD actually have worse fibrosis progression rates than their overweight counterparts, possibly because the disease is diagnosed later, and because the underlying genetic and metabolic drivers (insulin resistance, genetic variants like PNPLA3 and TM6SF2) operate independently of body weight.

If you are Indian, have normal weight, but also have a family history of diabetes or fatty liver, mildly elevated ALT, unexplained fatigue, or metabolic syndrome components (pre-diabetes, borderline triglycerides, low HDL) — then you need a liver assessment. Do not assume a normal body weight means a normal liver.

Symptoms — Why Most Patients Find Out by Accident

MASLD is, for most of its course, a silent disease. Simple steatosis and early MASH produce no symptoms. The liver has no pain receptors. By the time a patient experiences right upper quadrant discomfort, persistent fatigue, or a sense of abdominal fullness, significant fibrosis is often already present. By the time jaundice, leg swelling, or easy bruising appear, cirrhosis is established.

The majority of my patients who present with early MASLD find out via one of three routes: a routine blood test showing mildly elevated ALT or AST (often dismissed as “borderline” by a GP); an ultrasound for an unrelated reason that incidentally shows a bright echogenic liver; or a comprehensive health screen — increasingly common among NRI patients returning from abroad.

If you have metabolic risk factors, the right question is not “do I have symptoms?” but “what does my liver look like today?”

Red flags requiring urgent specialist referral: platelet count below 150,000 (possible portal hypertension); splenomegaly on imaging; spider naevi or palmar erythema; rising bilirubin or falling albumin; any HCC on surveillance imaging.

How MASLD Is Properly Diagnosed

Ultrasound: First Step, Not the Final Answer

An abdominal ultrasound can detect moderate-to-severe steatosis (grade 2–3) but misses early steatosis and — critically — tells you nothing about fibrosis. Two patients with identical ultrasound appearances can have F0 (no fibrosis) or F3 (bridging fibrosis) on biopsy. Ultrasound alone is not enough.

FibroScan (Transient Elastography): The Key Investigation

FibroScan measures liver stiffness — a direct correlate of fibrosis — using sound wave technology, painlessly, in under five minutes. It also quantifies the Controlled Attenuation Parameter (CAP), which grades fat content accurately.

It answers the question that changes clinical management: how stiff is your liver right now? A stiffness value above 8 kPa signals significant fibrosis; above 12 kPa, cirrhosis is likely. Combined with the FIB-4 index (derived from age, ALT, AST, and platelet count), we can stratify most patients into low, intermediate, and high risk without a biopsy.

FibroScan is available at Gleneagles Hospital, Mumbai.

Blood Tests

Standard panel: LFTs (ALT, AST, GGT, ALP, bilirubin, albumin, total protein), full blood count, fasting glucose, HbA1c, lipid profile, TSH. Calculate FIB-4 from these results at the first visit. Advanced fibrosis biomarker panels (Enhanced Liver Fibrosis score, Pro-C3) add precision when FIB-4 is intermediate (1.3–2.67).

When Liver Biopsy Is Still Needed

Biopsy remains the gold standard for staging, but is reserved for cases where non-invasive tests are discordant, where the diagnosis is uncertain (excluding autoimmune hepatitis, Wilson disease, or drug-induced injury), or where treatment trial enrolment requires histological confirmation. It is not routine.

Treatment — What Actually Works

The Foundation: Lifestyle Modification

No drug matches what a committed lifestyle change can achieve in early-to-moderate MASLD. A 7–10% reduction in body weight reliably reduces hepatic steatosis; ≥10% loss improves fibrosis in most patients with MASH.

Diet: The Mediterranean dietary pattern consistently outperforms low-fat diets. For Indian patients: replace refined grains (maida, white rice) with whole grains (jowar, bajra, brown rice); increase legumes (dal, rajma, chana); prioritise vegetables, olive oil or cold-pressed mustard oil, nuts; eliminate sugary beverages entirely; reduce fried and ultra-processed foods.

Exercise: 150 minutes/week of moderate aerobic activity combined with two to three sessions of resistance training produces greater liver fat reduction than either alone. Exercise improves insulin sensitivity independent of weight loss — this matters especially for lean MASLD patients.

Managing the Metabolic Comorbidities

Diabetes: GLP-1 receptor agonists (semaglutide, liraglutide) have demonstrated meaningful reduction in liver fat and histological improvement in MASH in Phase 3 trials. Semaglutide is available in India and increasingly prescribed jointly by hepatologists and endocrinologists.

Dyslipidemia: Statins are safe in MASLD. Many Indian patients refuse them fearing liver damage — the evidence is clear: statins reduce cardiovascular mortality in MASLD and do not worsen hepatic fibrosis.

Hypertension: RAAS-blocking agents (ACE inhibitors, ARBs) are preferred for their additional anti-fibrotic properties. Thyroid: Screen for hypothyroidism — a reversible metabolic driver of steatosis that is frequently missed.

Approved Pharmacotherapy

In March 2024, resmetirom (Rezdiffra) became the first FDA-approved drug specifically for MASH with liver fibrosis (F2–F3). It is a thyroid hormone receptor-β agonist targeting hepatic lipid metabolism directly. India approval is pending at the time of writing. Patients with significant fibrosis should be under specialist care to access these therapies as they become available.

The Transplant Prevention Conversation

This is the outcome that drives my urgency in evaluating and treating MASLD aggressively.

Data from the United States Scientific Registry of Transplant Recipients (SRTR) shows MASH-related cirrhosis is now the second most common indication for liver transplantation in the US and the most rapidly increasing — rising from 5% of transplant waitlist registrations in 2002 to 28% in 2019. Among women and patients over 54 years, MASH is already the leading indication.

For NRI patients, this is directly relevant. A significant proportion of Indian-origin patients reaching Western liver transplant centres with MASH cirrhosis had a diagnosis of “fatty liver” for 10–15 years — observed, not treated. The disease progressed silently through that window. The purpose of early evaluation is to close that window permanently. Every patient who achieves fibrosis regression through lifestyle and metabolic control is a patient who does not need a transplant discussion in ten years.

MASLD and the Diabetes-Liver Relationship: Why Your Endocrinologist Should Know Your FIB-4 Score

MASLD and type 2 diabetes are so tightly intertwined that managing one without awareness of the other is incomplete medicine. Insulin resistance — the metabolic root of both — simultaneously drives fat into the liver and prevents it from clearing normally. As MASLD progresses, the liver’s ability to regulate blood sugar deteriorates further, worsening glycaemic control and HbA1c.

This is why I recommend that every diabetic patient with MASLD have a formal liver assessment — FibroScan and FIB-4 — at least once, and annually if fibrosis is present. Physician-to-physician communication between hepatology and endocrinology matters.

For NRI Patients: Getting a Comprehensive Liver Assessment in India

For members of the Indian diaspora living in the UK, USA, Canada, UAE, Singapore, or Australia, a visit to India is often the opportunity to get investigations done efficiently, with expertise, at a fraction of the cost.

A comprehensive MASLD assessment at Gleneagles Hospital, Mumbai typically includes: full metabolic and liver blood panel (same-day results); FibroScan with CAP quantification; targeted abdominal ultrasound; clinical consultation with full risk stratification and a written management plan; and coordination with your home-country physician if required.

When Should You See a Hepatologist — Not Just a GP?

• ALT elevated on two separate occasions, even mildly (>30 U/L in women, >40 U/L in men)
• Fatty liver on ultrasound — any grade
• FIB-4 ≥1.30 (intermediate or indeterminate risk)
• Diabetes plus any liver enzyme abnormality
• Normal body weight but multiple metabolic risk factors
• Family history of cirrhosis or liver cancer
• Incidental thrombocytopenia (platelet count below 150,000)

You do not need symptoms to justify a hepatology consultation. You need risk factors — and by India’s metabolic disease burden, a large proportion of urban adults over 40 have at least one.

Frequently Asked Questions

What is the difference between NAFLD and MASLD?

They describe the same disease. NAFLD was the old name, used until 2023. MASLD is the current internationally agreed name, with clearer diagnostic criteria centred on metabolic risk factors. If you were told you have NAFLD, you now have what is called MASLD.

Can fatty liver be reversed completely?

Yes — in its early stages (steatosis and early MASH without significant fibrosis), MASLD is fully reversible with sustained lifestyle change and metabolic control. Significant fibrosis (F3) can regress but rarely disappears completely. Cirrhosis (F4) is generally not reversible, though its complications can be managed and its progression slowed.

What are the early signs of fatty liver in Indians?

Most people have no signs at all. The earliest detectable change is a mildly elevated ALT on a blood test, or a hyperechoic liver on ultrasound done for an unrelated reason. Early disease is diagnosed by investigation, not by symptoms.

Is fatty liver dangerous if you are not overweight?

Yes. Lean MASLD carries the same risk of fibrosis progression as MASLD in overweight patients, and may be detected later because the diagnosis is not suspected. Indians are particularly at risk due to lower BMI thresholds and high prevalence of genetic risk variants.

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This article is for educational purposes and does not replace a clinical consultation. To book a FibroScan or hepatology consultation with Dr. Chetan Kalal at Gleneagles Hospital, Mumbai, contact the outpatient department directly.

References

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2. Tokushige K. New concept in fatty liver diseases. Hepatol Res 2024. DOI: 10.1111/hepr.14004
3. Sato-Espinoza K et al. Update in lean MASLD. World J Hepatol 2024. DOI: 10.4254/wjh.v16.i3.452
4. Gupta U et al. MASLD: Current practice and screening guidelines. Am J Med Sci 2023. DOI: 10.1016/j.amjms.2023.11.007
5. GBD 2023 MASLD Collaborators. Global burden of MASLD 1990–2023. Lancet Gastroenterol Hepatol 2026. DOI: 10.1016/S2468-1253(26)00011-7
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8. Sood V et al. Practice Recommendations for MASLD by ISPGHAN. Indian Pediatr 2024. PMID: 39297398