Co-authored by: Dr Tim Trodd (Specialist in Family Medicine)
The Silent Problem Hiding in Plain Sight: Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)
Abdominal ultrasound is a routine part of a thorough medical check-up. One common finding is Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD, also known previously as NAFLD), which has quietly become one of the most common chronic liver conditions in the world, affecting an estimated 25 to 40% of the global population.[1]
Yet for most people, there are no symptoms, no warning signs, and no dramatic moment of diagnosis. One of the best reasons to have a regular medical check-up is precisely this, to look for MASLD before it becomes a serious problem.
What makes MASLD particularly sneaky is its deep connection to another largely invisible threat, visceral fat. This is not the soft, pinchable fat you can feel just beneath your skin. It is a more metabolically active type of fat that wraps around your internal organs, drains directly into your liver, and quietly disrupts your body's metabolism.
Understanding how these two conditions are connected is not merely an academic exercise. It is the foundation for effective treatment.
What Is Visceral Fat, and Why Does It Matter in Fatty Liver?
Visceral fat (medically known as visceral adipose tissue, or VAT) is fat deposited inside the abdominal cavity, surrounding organs like the liver, pancreas, and intestines. Unlike the soft layer of fat just beneath your skin, visceral fat is not passive storage. It behaves more like an active gland, constantly releasing fatty acids, inflammatory signals, and hormones that have a profound effect on your whole body metabolism.[2]
What makes visceral fat particularly dangerous is where it sits. This fat drains directly into the blood vessels that feed the liver, delivering a concentrated stream of fatty acids and inflammatory signals straight to it. This is now well established as a key reason why excess visceral fat leads to a fatty liver.[2]
Visceral fat is actually a stronger predictor of MASLD than BMI or total body fat, and has been consistently linked to advanced liver scarring even in people with a completely normal weight.[3,4]
This is a crucial and often overlooked point: you do not need to be overweight to have dangerous levels of visceral fat. Leaner people with excess visceral fat are at real risk of both MASLD and its serious long-term consequences.
Can You Have Fatty Liver If You Are Skinny? The Asian Risk Factor
For those of us in Hong Kong and across Asia, there is an additional and important layer of concern.
People of Asian ethnicity tend to accumulate more fat inside and around the liver at a lower body weight than their Western counterparts. This pattern is sometimes called the "Asian metabolic phenotype." Put simply, an Asian person and a Caucasian person with the same BMI and waist measurement will often have very different amounts of fat inside their liver and around their organs, with the Asian individual carrying significantly more of the harmful kind.[5]
This matters for two reasons.
First, the standard BMI thresholds used to define "overweight" and "obesity" were developed largely based on Western populations. For people of Asian ethnicity, health risks begin at a lower BMI, which is why Asian-specific thresholds have been recommended: overweight at a BMI of 23 or above, rather than the usual 25.[6]
Second, and perhaps more importantly, this means that MASLD can develop in people who appear slim by everyday standards. Across Asia, between 1 in 10 and 1 in 5 MASLD cases occur in people with a completely normal BMI.[7] Doctors and patients alike may not suspect a fatty liver problem if someone looks slim. That is precisely why an abdominal ultrasound or Fibroscan during a routine check-up is so valuable in this part of the world.
From Fatty Liver to Serious Complications: What Can Happen?
MASLD exists on a spectrum. For many people it stays mild, with fat in the liver but little inflammation and no immediate danger. But for a significant number, it progresses to a more serious stage called metabolic dysfunction-associated steatohepatitis (MASH), where the liver becomes inflamed and begins to scar.[8]
Left unaddressed, that scarring can advance toward:
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Cirrhosis: permanent liver scarring that stops the liver from working properly
-
Liver cancer: which can develop even in people who have not yet reached the stage of cirrhosis
-
Liver failure: in severe cases, requiring a transplant
Importantly, it is the amount of scarring, not the amount of fat, that most strongly determines long-term outcomes.[9]
But MASLD does not stop at the liver. It is now understood as a whole-body condition, and is independently linked to:[9,10]
-
Heart disease: one of the most significant risks, present regardless of weight, age, or smoking history
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Type 2 diabetes: a fatty liver and insulin resistance fuel each other in a damaging cycle
-
Kidney disease: people with MASLD have roughly twice the rate of chronic kidney disease[9]
-
Certain cancers: such as bowel cancer[8]
Visceral fat, meanwhile, adds its own layer of risk: worsening cholesterol levels, raising blood pressure, driving chronic inflammation throughout the body, and increasing the tendency for blood to clot.[11,12]
In short, MASLD and excess visceral fat are not two separate problems. They are two faces of the same metabolic crisis.
Dr Shiba Poon
- LMCHK
- MBBS (Lond)
- DRCOG
- DCH (RCPCH)
- PGDipClinDerm (Lond)
- MRCGP
- Honorary Clinical Assistant Professor In Family Medicine (HKU)
Health Articles by Dr Shiba Poon
References
- George, A. and Cobbold, J. (2023). Non-alcoholic fatty liver disease. Medicine, 51(5), pp. 336–341. https://doi.org/10.1016/j.mpmed.2023.02.003
- Ibrahim, M.M. (2010). Subcutaneous and visceral adipose tissue: structural and functional differences. Obesity Reviews, 11(1), pp. 11–18. https://doi.org/10.1111/j.1467-789X.2009.00623.x
- Ko, Y.H., et al. (2017). The correlation between body fat, visceral fat, and nonalcoholic fatty liver disease. Metab Syndr Relat Disord, 15(6), pp. 304–311. https://doi.org/10.1089/met.2017.0001
- Seaw, K.M., Henry, C.J. and Bi, X. (2023). Relationship between non-alcoholic fatty liver disease and visceral fat measured by imaging-based body composition analysis: a systematic review. Livers, 3(3), pp. 463–493. https://doi.org/10.3390/livers3030033
- Wulan, S.N., Westerterp, K.R. and Plasqui, G. (2010). Ethnic differences in body composition and the associated metabolic profile: a comparative study between Asians and Caucasians. Maturitas, 65(4), pp. 315–319. https://www.sciencedirect.com/science/article/abs/pii/S0378512209004678
- WHO Expert Consultation. (2004). Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies. The Lancet, 363(9403), pp. 157–163. https://doi.org/10.1016/S0140-6736(03)15268-3
- Albusta, N., Isa, S. and Alrahma, H. (2026). Lean Metabolic-Dysfunction-Associated Steatotic Liver Disease (MASLD): Pathophysiology, Diagnostic Challenges, Clinical Outcomes, and Management. Diseases, 14(5), article 173. https://doi.org/10.3390/diseases14050173
- European Association for the Study of the Liver, European Association for the Study of Diabetes and European Association for the Study of Obesity. (2016). EASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. J Hepatol, 64(6), pp. 1388–1402. https://doi.org/10.1016/j.jhep.2015.11.004
- Rinella, M.E., et al. (2023). AASLD Practice Guidance on the clinical assessment and management of nonalcoholic fatty liver disease. Hepatology, 77(5), pp. 1797–1835. https://doi.org/10.1097/HEP.0000000000000323
- Shahid, I., et al. (2025). Obesity and atherosclerotic cardiovascular disease: a review of social and biobehavioural pathways. Methodist Debakey Cardiovasc J, 21(2), pp. 23–34. https://doi.org/10.14797/mdcvj.1528
- Cesaro, A., et al. (2023). Visceral adipose tissue and residual cardiovascular risk: a pathological link and new therapeutic options. Front Cardiovasc Med, 10, p. 1187735. https://doi.org/10.3389/fcvm.2023.1187735
- Mertens, I. and Van Gaal, L.F. (2002). Obesity, haemostasis and the fibrinolytic system. Obes Rev, 3(2), pp. 85–101. https://doi.org/10.1046/j.1467-789X.2002.00056.x
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