
Every 14 November, India faces a number that gets harder to ignore. The latest national ICMR-INDIAB survey estimated that 101 million Indians are living with diabetes, and another 136 million have prediabetes [1].
Those numbers are huge. But I don’t think about them as numbers. I think about the people behind them, because I meet them every week.
I’ve spent many years counselling people about their liver and their blood sugar. And I’ve noticed a pattern. When we talk about diabetes, we talk about sugar, weight and family history. We almost never ask where the trouble begins.
For many Indians, part of the answer lies in the liver. The changes start quietly. Often, they begin years before a blood sugar report looks worrying.
So if you’ve been told you have fatty liver, I wrote this World Diabetes Day 2026 article for you.
Is Fatty Liver Dangerous?
Picture this. You’ve just had a routine ultrasound. The report says “Grade 1 fatty liver” or perhaps “Grade 2”. Your doctor tells you to watch your diet. You nod, go home, and then search late at night: is fatty liver dangerous?
You’re not alone. It’s the first question almost everyone asks me.
Yes, it can be.
A Grade 1 or Grade 2 result won’t harm you overnight. The real concern is something most people are never told. Fatty liver is strongly associated with insulin resistance, and it can contribute to it. Insulin resistance is a slow shift in how your body handles sugar. Over time, it can lead to prediabetes and type 2 diabetes [2,3].
You might also hear your doctor use a newer name for the condition: MASLD. It stands for metabolic dysfunction-associated steatotic liver disease [2]. A mouthful, I know. It simply means fat in the liver that’s linked to how your body processes energy.
Your Liver as a Dormant Volcano
When I explain this to my clients, I use one picture. A dormant volcano.
From the outside, everything looks calm. No smoke. No rumbling. You feel more or less fine.
But underneath, low-grade inflammation can build pressure. Quietly. Year after year.
And you may already be feeling a few early tremors. These signs of insulin resistance are common. None of them means you have a problem on its own, but together they’re worth noticing:
- Feeling heavy and tired after meals, especially after a plate of rice or a few rotis
- Belly fat that just won’t shift, even when your weight stays the same
- Fasting sugar creeping up at each check-up. A fasting glucose of 100–125 mg/dL or an HbA1c of 5.7–6.4% falls in the prediabetes range [4]
- Rising triglycerides or falling HDL (“good”) cholesterol on your lipid report
- Darker, velvety patches of skin on the neck or underarms
Do any of these sound familiar? If so, keep reading. By the end of this article, you’ll know three things:
- What may be happening inside your liver cells
- Which numbers to keep an eye on
- What you can start doing today
Fatty Liver Complications: How Dangerous Is Fatty Liver, Really?
When people see the word “mild” on their report, they relax. I completely understand. Who wouldn’t?
But in my years of practice, I’ve learned that mild doesn’t mean harmless. Fatty liver is common. It’s usually silent. And it’s closely tied to your blood sugar.
Let me show you what I mean.
The numbers behind my concern
| What the research tells us | Figure | Source |
|---|---|---|
| Indians living with diabetes | 101 million | [1] |
| Indians living with prediabetes | 136 million | [1] |
| Indian adults with fatty liver (pooled national estimate) | About 39%, or roughly 2 in 5 | [5] |
| Indian adults with fatty liver (earlier community studies) | 9–32% | [6] |
| Indians with type 2 diabetes who have fatty liver (national SPRINT study) | More than half | [7] |
| People worldwide with type 2 diabetes who have fatty liver | About 55% | [8] |
| Adults worldwide with fatty liver | About 25%, with recent estimates nearing 1 in 3 | [9,10] |
Two things jump out at me. First, our Indian figures sit at or above global levels. Second, fatty liver and diabetes turn up together far too often to be a coincidence.
I see this overlap every day in my clinic. And it’s especially clear in people over 50.
Fatty liver and diabetes: the biggest risk
Here’s the finding I share most often. A meta-analysis of more than 500,000 adults found that people with fatty liver were roughly twice as likely to develop type 2 diabetes as people without it [11].
Twice as likely. That’s worth sitting with for a moment.
There’s more. Studies show that fat often builds up in the liver before blood sugar starts to rise. Many researchers now see liver fat as an early marker of the process that leads to type 2 diabetes, not just a result of it [12].
That’s why I tell my patients this: think of your fatty liver as an early warning light on your dashboard. It often comes on before your glucometer shows anything at all.
It’s not only about blood sugar
Fatty liver can affect more than your sugar levels:
- Your heart: Fatty liver is linked to a higher risk of heart attack, stroke and other cardiovascular problems [13].
- Your liver itself: If inflammation carries on unchecked, fatty liver can progress to steatohepatitis (MASH) and then to fibrosis. Fibrosis means the liver tissue becomes stiff and scarred, and it’s much harder to reverse [14].
So, is fatty liver disease dangerous? Let me put it simply. At Grade 1 or 2, it’s a warning, not an emergency. But if you ignore it, it can become the starting point for some of the most serious health problems adults over 50 face.
The good news? A warning gives you time. And time is exactly what you need.
Inside the Dormant Volcano: How Fatty Liver Insulin Resistance Develops
This is the part I most want you to understand. Hardly anyone has it explained to them. And you don’t need a science background to follow it, I promise.
Think of your liver as your body’s main chemical factory. It processes fats. It stores sugar and releases it when you need it. It packs up nutrients and sends them around your body.
When fat and inflammation build up, the factory’s production lines can start to falter. One by one. It’s not a fixed set of steps that happens the same way in everyone. Each person has their own family history and epigenetics which impacts the speed of changes and type of changes in the liver metabolism.
Stage 1: The accumulation of tiny fat droplets (fat builds up in liver cells)
When your liver gets more sugar and fat than it can handle, it doesn’t throw the extra away. It stores it as tiny fat droplets inside your liver cells.
Once at least 5% of your liver cells hold these droplets, it’s called fatty liver [15]. That’s the Grade 1 or Grade 2 you saw on your ultrasound report.
Stage 2: The walls weaken (cell membranes change)
Every liver cell is wrapped in a soft, flexible outer wall called a membrane. It’s made mostly of fats called phospholipids. The most plentiful of these is phosphatidylcholine, or PC for short.
A healthy membrane needs the right balance between PC and another phospholipid called PE. In laboratory studies, when this PC:PE ratio dropped, the membranes became weaker, and this was linked to liver inflammation [16]. And in human studies, people with fatty liver tend to have a lower PC:PE ratio, both in the liver and in their red blood cells [17].
In plain words? The walls of your liver cells get flimsy.
Stage 3: Pressure builds (silent inflammation)
Now the cells are stressed and full of fat. So they start sending out distress signals. The liver’s own immune cells hear them and rush in.
At the same time, harmful molecules called reactive oxygen species pile up. This is known as oxidative stress, and it can damage the inside of your cells [14,18].
This is the dormant volcano at work. You feel no pain. You have no fever. There’s just a steady, low burn underneath.
And here’s the key link. Over time, those inflammatory signals can get in the way of the messages insulin uses to talk to your cells [3,19]. Like static on a phone line.
Stage 4: The production lines falter (biochemical pathways disrupted)
As the cell walls weaken and the inflammation simmers, research points to four parts of the liver factory that can start to go wrong:
- The fat-export lorries stall (VLDL secretion). Your liver sends fat out in little parcels called VLDL. To build them, it needs phosphatidylcholine. When PC runs low, fewer parcels leave, and more fat stays stuck inside [16,18].
- The fat-making switch gets stuck “on” (SREBP-1). SREBP-1 works like a master switch for making new fat. In experimental studies, low PC pushes this switch on, so the liver makes even more fat [18,20].
- The fat-burning furnace dims (PPAR-α). PPAR-α tells your liver to burn fat for energy. Laboratory research has found that a specific phosphatidylcholine molecule acts as one of its natural “keys” [21]. With fewer keys around, less fat may get burned.
- The scarring cells wake up (stellate cell activation). Ongoing damage switches on cells that lay down scar tissue. That’s the first step towards fibrosis [14,18].
Can you see how it all feeds itself? More fat brings more inflammation. Inflammation weakens your insulin response. And a weaker insulin response encourages even more fat storage [3,18].
It’s a vicious circle. But circles can be broken.
Stage 5: The inflammation triggers (insulin resistance becomes prediabetes)
Normally, after you eat, insulin tells your liver, “That’s enough sugar, stop releasing it now.”
A fatty, inflamed liver may not hear that message clearly. So it keeps sending glucose into your bloodstream [3]. Your pancreas notices and works harder to make more insulin.
Over months and years, this insulin resistance in the liver can spread to the rest of your body. Your fasting sugar rises. Your HbA1c creeps up. And prediabetes may follow [3].
Left alone, the inflammation triggers might lead to type 2 diabetes, MASH, or both [3,14].
Precautions: What You Can Do, Starting Today
This is where I want you to feel hopeful. Truly.
In my practice, I’ve watched how quickly the liver responds when you give it the right conditions. It’s a remarkably forgiving organ. Early-stage fatty liver is often reversible with steady lifestyle changes [15].
You don’t need a perfect diet. You don’t need a gym membership. You just need to start.
Six steps to protect your liver and your blood sugar
- Cut back on refined carbs and added sugar. White rice, maida, sugary chai, biscuits and sweet drinks all put extra strain on your liver. Try swapping in whole grains, millets, dals and plenty of vegetables. Small changes you can keep up beat a strict diet you’ll drop in two weeks.
- Move every day, and lift twice a week. Aim for at least 30 minutes of brisk walking, or something similar, each day. Then add some resistance exercise twice a week. Bands, light weights or simple bodyweight moves all count. Being active can reduce liver fat and help your body use insulin better, even before you lose any weight [15].
- Lose a little weight, slowly, if you’re carrying extra. Losing just 5–7% of your body weight can make a real difference to liver fat. If you weigh 75 kg, that’s around 4–5 kg. Larger losses bring even more benefit for inflammation and scarring [15,22].
- Watch your waist, not just the scale. Belly fat is closely tied to liver fat. This matters a lot in India, where many people develop fatty liver at a “normal” weight [23]. Worldwide, around 40% of people with fatty liver aren’t obese at all [24]. So grab a measuring tape too.
- Add choline-rich foods to your plate. Your body uses choline to make phosphatidylcholine, the very building block your liver cell walls need. In a controlled study, most men and postmenopausal women put on a low-choline diet developed fatty liver or other organ problems. Once choline went back into their diet, these problems cleared up [25]. The adequate intake is 550 mg a day for men and 425 mg a day for women [26]. Eggs, fish, soy, legumes and leafy greens are all good sources.
- Get tested once a year. Ask for HbA1c and fasting glucose alongside your liver tests. These simple blood tests can spot rising blood sugar long before you feel anything [4].
Common mistakes I see (and how to avoid them)
- Waiting until you feel unwell. Fatty liver rarely hurts. Let your numbers guide you, not how you feel.
- Trusting a normal BMI. Being slim doesn’t rule out liver fat. Measure your waist as well.
- Trying to change everything at once. Crash diets almost never last. Pick one change this week. Just one. Then build from there.
Supporting Your Liver Cells at the Root: Essential Phospholipids
Remember those flimsy cell walls from Stage 2? This is where nutritional support may help.
Essential Phospholipids (EPL) are highly purified phosphatidylcholine molecules taken from soybean. Their star ingredient is DLPC (dilinoleoylphosphatidylcholine). In therapeutic-grade EPL, DLPC can make up as much as 52% of the phosphatidylcholine [18]. In your blood, DLPC is normally only a small part of your phosphatidylcholine. Research shows that taking EPL by mouth can raise its levels in your cell membranes [27].
Why does that matter? Because phosphatidylcholine sits right at the centre of every problem we talked about. Research, much of it experimental, suggests that topping it up may help your liver in several ways:
- Stronger cell walls: It may help rebuild membrane structure and flexibility, which supports the receptors and enzymes that sit in those walls [18,27].
- Less fat-making: It may help calm that stuck “on” fat-making switch (SREBP-1) [18,20].
- More fat-burning: It may support fat burning through PPAR-α [18,21].
- Better fat export: It may help your liver send fat out through VLDL [16,18].
- Less oxidative stress: It may help reduce oxidative stress, which is linked to inflammation and scarring [28].
What the clinical studies show
I always want to show you the evidence, not just tell you a story. So here’s what research has found:
- A systematic review and network meta-analysis: In people with fatty liver and type 2 diabetes or obesity, adding EPL to diabetes medicine worked better than medicine alone. ALT, a liver enzyme, fell by an extra 11.28 U/L. Triglycerides fell by an extra 49.33 mg/dL. And the chance of overall improvement was 50% higher (RR 1.50, P < 0.0001) [28]. That said, many of the trials were small, so we still need bigger, well-designed studies.
- The MANPOWER study (2,843 adults): People with fatty liver and conditions like diabetes or high blood pressure took 1.8 g of polyenylphosphatidylcholine daily, alongside their usual care, for 24 weeks. Liver echogenicity, an ultrasound sign of liver fat, improved in 68.3% of them. Among those whose scans were abnormal at the start, 81.4% improved. The results held steady across people with diabetes, high blood pressure, high cholesterol and obesity [29]. To be fair, this was a real-world study without a comparison group. So it adds to controlled trials rather than replacing them.
Where Meru Activs Fatty Liver Support fits in
Meru Activs Fatty Liver Support is made specifically for adults over 50. It’s powered by LECIVA-S40L, a soy-derived source of Essential Phospholipids, and gives 1,260 mg of phospholipids a day. The studies above tested Essential Phospholipids as an ingredient, at their own doses.
Its aim is simple. To support the health of your liver cell membranes, the same walls that are at the heart of this whole story. It’s designed to work alongside the food and movement changes above, never in place of them.
Two things I’d love you to do this World Diabetes Day
This World Diabetes Day, add one test to your next appointment. Ask for HbA1c and fasting glucose alongside your next ultrasound or LFT. It’s one extra box on the same form.
And if you want to support your liver cells at the level where this all begins, this is what Meru Activs Fatty Liver Support is designed to do.
And if you’re reading this for your mum or dad? Share it with them. Then book that test together. It means more coming from you.
Frequently Asked Questions
Is fatty liver dangerous?
Can fatty liver cause diabetes?
Is fatty liver a sign of prediabetes?
Can you have fatty liver without being overweight?
Is fatty liver reversible?
What is the difference between NAFLD and MASLD?
References
References are numbered in order of first citation (Vancouver style) and grouped by evidence tier.
- Anjana RM, Unnikrishnan R, Deepa M, et al. Metabolic non-communicable disease health report of India: the ICMR-INDIAB national cross-sectional study (ICMR-INDIAB-17). Lancet Diabetes Endocrinol. 2023;11(7):474–89. doi:10.1016/S2213-8587(23)00119-5
- Rinella ME, Lazarus JV, Ratziu V, et al. A multisociety Delphi consensus statement on new fatty liver disease nomenclature. J Hepatol. 2023;79(6):1542–56. doi:10.1016/j.jhep.2023.06.003
- Samuel VT, Shulman GI. Nonalcoholic fatty liver disease as a nexus of metabolic and hepatic diseases. Cell Metab. 2018;27(1):22–41. doi:10.1016/j.cmet.2017.08.002
- American Diabetes Association Professional Practice Committee. 2. Diagnosis and classification of diabetes: Standards of Care in Diabetes: 2025. Diabetes Care. 2025;48(Suppl 1):S27–49. doi:10.2337/dc25-S002
- Shalimar, Elhence A, Bansal B, et al. Prevalence of non-alcoholic fatty liver disease in India: a systematic review and meta-analysis. J Clin Exp Hepatol. 2022;12(3):818–29. doi:10.1016/j.jceh.2021.11.010
- Duseja A. Nonalcoholic fatty liver disease in India – a lot done, yet more required! Indian J Gastroenterol. 2010;29(6):217–25. doi:10.1007/s12664-010-0069-1
- Kalra S, Vithalani M, Gulati G, et al. Study of prevalence of nonalcoholic fatty liver disease (NAFLD) in type 2 diabetes patients in India (SPRINT). J Assoc Physicians India. 2013;61(7):448–53. PMID: 24772746.
- Younossi ZM, Golabi P, de Avila L, et al. The global epidemiology of NAFLD and NASH in patients with type 2 diabetes: a systematic review and meta-analysis. J Hepatol. 2019;71(4):793–801. doi:10.1016/j.jhep.2019.06.021
- Younossi ZM, Koenig AB, Abdelatif D, et al. Global epidemiology of nonalcoholic fatty liver disease: meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology. 2016;64(1):73–84. doi:10.1002/hep.28431
- Riazi K, Azhari H, Charette JH, et al. The prevalence and incidence of NAFLD worldwide: a systematic review and meta-analysis. Lancet Gastroenterol Hepatol. 2022;7(9):851–61. doi:10.1016/S2468-1253(22)00165-0
- Mantovani A, Petracca G, Beatrice G, et al. Non-alcoholic fatty liver disease and risk of incident diabetes mellitus: an updated meta-analysis of 501 022 adult individuals. Gut. 2021;70(5):962–9. doi:10.1136/gutjnl-2020-322572
- Taylor R. Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause. Diabetologia. 2008;51(10):1781–9. doi:10.1007/s00125-008-1116-7
- Targher G, Byrne CD, Lonardo A, et al. Non-alcoholic fatty liver disease and risk of incident cardiovascular disease: a meta-analysis. J Hepatol. 2016;65(3):589–600. doi:10.1016/j.jhep.2016.05.013
- Tilg H, Moschen AR. Evolution of inflammation in nonalcoholic fatty liver disease: the multiple parallel hits hypothesis. Hepatology. 2010;52(5):1836–46. doi:10.1002/hep.24001
- European Association for the Study of the Liver (EASL), European Association for the Study of Diabetes (EASD), European Association for the Study of Obesity (EASO). EASL–EASD–EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD). J Hepatol. 2024;81(3):492–542. doi:10.1016/j.jhep.2024.04.031
- Li Z, Agellon LB, Allen TM, et al. The ratio of phosphatidylcholine to phosphatidylethanolamine influences membrane integrity and steatohepatitis. Cell Metab. 2006;3(5):321–31. doi:10.1016/j.cmet.2006.03.007
- Arendt BM, Ma DW, Simons B, et al. Nonalcoholic fatty liver disease is associated with lower hepatic and erythrocyte ratios of phosphatidylcholine to phosphatidylethanolamine. Appl Physiol Nutr Metab. 2013;38(3):334–40. doi:10.1139/apnm-2012-0261
- Osipova D, Kokoreva K, Lazebnik L, et al. Regression of liver steatosis following phosphatidylcholine administration: a review of molecular and metabolic pathways involved. Front Pharmacol. 2022;13:797923. doi:10.3389/fphar.2022.797923
- Hotamisligil GS. Inflammation and metabolic disorders. Nature. 2006;444(7121):860–7. doi:10.1038/nature05485
- Walker AK, Jacobs RL, Watts JL, et al. A conserved SREBP-1/phosphatidylcholine feedback circuit regulates lipogenesis in metazoans. Cell. 2011;147(4):840–52. doi:10.1016/j.cell.2011.09.045
- Chakravarthy MV, Lodhi IJ, Yin L, et al. Identification of a physiologically relevant endogenous ligand for PPARα in liver. Cell. 2009;138(3):476–88. doi:10.1016/j.cell.2009.05.036
- Vilar-Gomez E, Martinez-Perez Y, Calzadilla-Bertot L, et al. Weight loss through lifestyle modification significantly reduces features of nonalcoholic steatohepatitis. Gastroenterology. 2015;149(2):367–78.e5. doi:10.1053/j.gastro.2015.04.005
- Das K, Das K, Mukherjee PS, et al. Nonobese population in a developing country has a high prevalence of nonalcoholic fatty liver and significant liver disease. Hepatology. 2010;51(5):1593–602. doi:10.1002/hep.23567
- Ye Q, Zou B, Yeo YH, et al. Global prevalence, incidence, and outcomes of non-obese or lean non-alcoholic fatty liver disease: a systematic review and meta-analysis. Lancet Gastroenterol Hepatol. 2020;5(8):739–52. doi:10.1016/S2468-1253(20)30077-7
- Fischer LM, daCosta KA, Kwock L, et al. Sex and menopausal status influence human dietary requirements for the nutrient choline. Am J Clin Nutr. 2007;85(5):1275–85. doi:10.1093/ajcn/85.5.1275
- Zeisel SH, da Costa KA. Choline: an essential nutrient for public health. Nutr Rev. 2009;67(11):615–23. doi:10.1111/j.1753-4887.2009.00246.x
- Gundermann KJ, Kuenker A, Kuntz E, et al. Activity of essential phospholipids (EPL) from soybean in liver diseases. Pharmacol Rep. 2011;63(3):643–59. doi:10.1016/S1734-1140(11)70576-X
- Dajani AI, Popovic B. Essential phospholipids for nonalcoholic fatty liver disease associated with metabolic syndrome: a systematic review and network meta-analysis. World J Clin Cases. 2020;8(21):5235–49. doi:10.12998/wjcc.v8.i21.5235
- Maev IV, Samsonov AA, Palgova LK, et al. Effectiveness of phosphatidylcholine in alleviating steatosis in patients with non-alcoholic fatty liver disease and cardiometabolic comorbidities (MANPOWER study). BMJ Open Gastroenterol. 2020;7(1):e000341. doi:10.1136/bmjgast-2019-000341
Meru Activs™: World Diabetes Day Blog Series 2026. Written by Dt. Sheetal Ruparel Somaiya.
Disclaimer: This article is for general information and education only. It does not constitute medical advice, diagnosis or treatment. Always consult a qualified doctor or registered dietitian before changing your diet, exercise routine, medication or supplement regimen, especially if you have diabetes, liver disease or any other health condition. Meru Activs Fatty Liver Support is a health supplement and is not for medicinal use. It is not intended to diagnose, treat, cure or prevent any disease. It should not be used as a substitute for a varied, balanced diet or for prescribed medical treatment. Do not exceed the recommended daily usage. Keep out of reach of children.