84% of Indian IT employees have fatty liver disease. Cutting calories won’t fix it

In 'Sick Nation', Karan Sarin offers a proactive, preventative protocol for metabolic health—designed to detect and address insulin resistance in Indians.

Representational image | Flickr

Think of your liver as the busy parent in a large household—involved in everything, managing countless operations simultaneously, and utterly essential to keeping the family functioning. Nothing metabolic happens without the liver’s participation. This remarkable organ handles every nutrient type, whether making them, storing them, or burning them for energy.

The liver’s unparalleled metabolic versatility makes it uniquely vulnerable. It can process proteins, carbohydrates, and fats with equal expertise. It manufactures essential compounds, detoxifies harmful substances, and serves as our primary glucose regulator. Yet for all its resilience, the liver has one critical vulnerability: it was never designed to be a long-term fat storage depot.

When insulin resistance takes hold, this vulnerability becomes painfully apparent. The liver, constantly bathed in elevated insulin levels, receives conflicting metabolic signals that fundamentally alter how it processes and stores energy.

Most people discover they have fatty liver during routine blood tests or ultrasounds done for other reasons. You might notice slightly elevated liver enzymes (ALT and AST) on your blood report, or your doctor might mention seeing “hepatic steatosis” on an ultrasound. Many patients are simply told to “lose weight and cut back on fatty foods” without any explanation of the metabolic processes driving their condition.

Building on our understanding of insulin’s role in hepatic metabolism discussed earlier, insulin resistance creates a “perfect storm” for fat accumulation in the liver through multiple interconnected pathways:

1. Free Fatty Acid Uptake: In normal metabolism, fat cells (adipo-cytes) release stored fat as free fatty acids only when insulin levels are low, like during fasting. However, when fat cells become insu-lin-resistant, they ignore insulin’s signal to hold onto fat.20 Think of it like this: insulin normally acts as a traffic officer, telling fat cells to hold onto their fat. But in insulin resistance, the fat cells stop listening to this officer, releasing fat into the bloodstream even when they’re being signaled not to.
2. Fat Manufacturing: Simultaneously, the liver creates its own fat when excess carbohydrates (particularly fructose) overwhelm its storage capacity. This process, called de novo lipogenesis, involves converting carbohydrates directly into fatty acids. Imagine your liver as a factory that typically produces essential proteins and manages glucose. When flooded with excess carbohydrates, this factory shifts to producing fat instead—a function it wasn’t primarily designed to handle. In people with fatty liver disease, this fat production pathway becomes dramatically overactive.
3. Impaired Fat Burning: High insulin levels command the liver to store rather than burn fat. This fundamental principle explains why fasting, which rapidly lowers insulin, can reduce liver fat—it finally allows the liver to access and burn stored fat.
4. Compromised Fat Export: The liver typically packages excess fat into very low-density lipoproteins (VLDL) for distribution to other tissues. Insulin resistance can impair this process, further contributing to fat retention within the liver.23

This four-part problem creates a dangerous contradiction: high insulin levels force the liver to store fat rather than burn it, while insu-lin-resistant fat cells supply an endless stream of fatty acids despite these elevated insulin levels. It’s like trying to empty a bathtub while the tap is running full blast and the drain is partially clogged.

Many patients tell me they’ve been frustrated after being told simply to “eat less fat” to treat their fatty liver. Now you can see why this advice makes little sense—the problem isn’t about eating fat; it’s about an insulin-resistant body forcing the liver to create and store fat.

This explains the tragic gap in my own brother-in-law’s care. He was diagnosed with fatty liver five years before he died and given the standard, tragically inadequate advice: lose some weight and cut back on dietary fat. No one explained to him that the real problem wasn’t the ghee on his roti, but the roti under his ghee—the ‘invisible sugars’ from carbohydrates like refined flour that his insulin-resistant body was turning into the very fat that was damaging his liver.

While all carbohydrates can drive insulin-mediated fat storage in the liver, fructose deserves special attention. Unlike glucose, which can be metabolized by virtually every cell in the body, fructose is primarily processed in the liver. This places a unique metabolic burden on this vital organ.

When fructose enters the liver, it bypasses key regulatory steps in metabolism and directly enters the pathways that promote fat formation. Every molecule of fructose metabolized by the liver results in molecular changes that promote fat storage and reduce fat burning. This helps explain why sugar-sweetened beverages, which typically contain high amounts of fructose as high-fructose corn syrup or sucrose (which breaks down into glucose and fructose), are particularly harmful to liver health.

Research has demonstrated that even modest consumption of fructose-sweetened beverages for just a few weeks can significantly increase liver fat content and accelerate fat production in the liver. These effects occur even before any significant weight gain becomes apparent, highlighting fructose’s direct influence on liver metabolism independent of its caloric content.

A simple action step: Replace sugary beverages (including fruit juices) with water or unsweetened tea. This single change can dramatically reduce the fructose burden on your liver, but it’s crucial to under-stand that the accumulation of fat is only the beginning.

The real damage starts when the liver reacts to this burden. As fat accumulates in the liver, it doesn’t simply sit there inertly. The fat-laden liver cells become metabolically stressed, triggering a cascade of inflammatory responses. This transition from simple fat accumulation (steatosis) to inflammation (steatohepatitis) represents a critical turning point in the disease process.

Several mechanisms contribute to this inflammatory response:

1. Toxic Fat Effects: When liver cells become overloaded with certain types of fat, particularly saturated fats created through the liver’s own fat production, these fats can directly damage cellular structures, like trying to store cooking oil in a paper bag.
2. Oxidative Stress: Fat-laden liver cells produce increased amounts of harmful reactive molecules (similar to what causes metal to rust), damaging cellular components and triggering inflammatory responses.
3. Cellular Factory Disruption: The accumulation of fat disrupts the normal functioning of the liver cell’s protein-making machinery (called the endoplasmic reticulum), leading to stress responses that promote inflammation.
4. Immune System Activation: Various immune cells, including the liver’s resident defense cells, become activated in response to these stressors, releasing inflammatory signaling molecules throughout the liver.

This inflammatory environment is what distinguishes simple fatty liver from the more serious non-alcoholic steatohepatitis (NASH). While simple fatty liver has a relatively benign course, NASH significantly increases the risk of progression to scarring (fibrosis), severe scarring (cirrhosis), and even liver cancer. Importantly, it’s this same inflammatory environment that creates elevated cardiovascular risk, helping explain why my brother-in-law, with his fatty liver disease, ultimately succumbed to a cardiac event.

This danger is particularly acute for Indians, who appear especially susceptible to fatty liver disease. Some studies suggest prevalence rates between 30%-40% in urban populations. The IT industry seems especially affected—a study conducted in 2023 and 2024 by the University of Hyderabad found that a staggering 84% of IT employees have fatty liver disease. Several factors contribute to this elevated risk:

1. The “Thin-Fat” Phenotype: As discussed in previous chapters, Indians tend to have higher body fat percentages and more visceral fat at lower BMIs compared to Western populations. This predisposes us to insulin resistance and fat accumulation in the liver even when we don’t appear obviously overweight. This is a critical point—you don’t need to be overweight to have fatty liver disease if you’re Indian.
2. Genetic Factors: Certain genetic variants that affect fat metabolism and insulin signaling appear more common in South Asian populations, potentially increasing susceptibility to liver fat accumulation.
3. Dietary Patterns: The rapid nutrition transition in India has led to increased consumption of refined carbohydrates and pro-cessed foods while maintaining traditionally high carbohydrate intake patterns. This combination is particularly problematic for liver health.
4. Sedentary Lifestyle: Decreasing physical activity levels in urban India further reduce insulin sensitivity and compromise the liver’s ability to process nutrients efficiently.

These factors help explain why seemingly healthy, non-obese Indians often receive shocking diagnoses of fatty liver disease. Many patients tell me they’re baffled—”But Karan, I don’t drink alcohol, I’m not overweight, I eat home-cooked food…” Now you can understand why those factors alone aren’t protective in our genetic and environmental context.

This excerpt from ‘Sick Nation’ by Karan Sarin has been published with permission from Wyzr Content.