84% of Indian IT employees have fatty liver disease

TThe liver is like a busy parent in a large family. They are involved in everything, manage a myriad of tasks at the same time, and are essential to keeping the family functioning. Nothing in metabolism occurs without the involvement of the liver. This remarkable organ processes all kinds of nutrients, including making them, storing them, and burning them for energy.

The liver has unique vulnerabilities due to its unparalleled metabolic diversity. Process proteins, carbohydrates, and fats with equal expertise. It manufactures essential compounds, detoxifies harmful substances, and acts as a major glucose regulator. But despite its resilience, the liver has one major vulnerability. That said, the liver isn’t designed to be a long-term fat store.

Most people discover they have fatty liver during routine blood tests or ultrasounds done for other reasons. You may notice slightly elevated liver enzymes (ALT and AST) in your blood tests. Your doctor may also mention that an ultrasound shows a “fatty liver.” Many patients are simply told to “lose weight and eat fewer fatty foods” without any explanation of the metabolic processes that cause their condition.

Given the previously discussed understanding of insulin’s role in hepatic metabolism, insulin resistance creates a “perfect storm” for fat accumulation in the liver through multiple interrelated pathways.

1. Free fatty acid uptake: In normal metabolism, adipocytes (adipocytes) release their stored fat as free fatty acids only when insulin levels are low, such as during fasting. However, when fat cells become insulin resistant, they ignore insulin’s signals to retain fat20. Think of it like this: Insulin normally acts as a traffic cop, telling fat cells to hold on to fat. However, when insulin resistance develops, fat cells no longer listen to this police officer and release fat into the bloodstream even when signals are being given that they shouldn’t.
2. Oil and fat manufacturing: At the same time, when excess carbohydrates (especially fructose) exceed the liver’s storage capacity, the liver produces its own fat. This process, called de novo lipogenesis, involves the direct conversion of carbohydrates into fatty acids. Imagine that the liver is normally a factory that produces essential proteins and manages glucose. When flooded with excess carbohydrates, this factory shifts to producing fat instead, something it wasn’t originally designed to handle. In people with fatty liver disease, this lipogenic pathway becomes dramatically overactive.
3. Disorders of fat burning: High insulin levels tell the liver to store fat instead of burning it. This basic principle explains why fasting, which rapidly lowers insulin, reduces liver fat. This ultimately allows the liver to access and burn stored fat.
4. Exporting fat at risk: The liver normally packages excess fat into very low density lipoproteins (VLDL) for distribution to other tissues. Insulin resistance may impair this process, further promoting fat retention within the liver23.

This four-part problem creates a dangerous contradiction. High insulin levels cause the liver to store fat instead of burning it, but insulin-resistant fat cells have an endless supply of fatty acids despite elevated insulin levels. It’s like trying to empty a bathtub when the drain is partially clogged while the faucet is running at full capacity.

Many patients tell me they are frustrated when they are simply told to “reduce their fat intake” in order to treat fatty liver disease. Now you can see why this advice makes little sense. The problem isn’t eating fat. It’s about an insulin-resistant body forcing the liver to produce 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 his death and was given standard and tragically inadequate advice to lose weight and reduce fat in his diet. no one explained to him the real problem There was roti under ghee instead of ghee on top of roti.His insulin-resistant body turned the “invisible sugar” contained in carbohydrates such as refined flour into fat, damaging his liver.

All carbohydrates can promote insulin-mediated fat accumulation in the liver, but fructose requires special attention. Unlike glucose, which can be metabolized by nearly every cell in the body, fructose is primarily processed by the liver. This places a unique metabolic load on this vital organ.

When fructose enters the liver, it bypasses important regulatory steps in metabolism and enters directly into 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 sugary drinks, which typically contain large amounts of fructose, such as high fructose corn syrup and sucrose (which breaks down into glucose and fructose), are particularly harmful to liver health.

Studies have demonstrated that even modest consumption of fructose-sweetened beverages for just a few weeks significantly increases liver fat content and stimulates liver lipogenesis. These effects occur even before a significant increase in body weight is evident, highlighting the direct effects of fructose on liver metabolism, independent of fructose’s caloric content.

Simple action steps: Replace sugary drinks (including fruit juices) with water or unsweetened tea. This one change can dramatically reduce the fructose burden on your liver, but it’s important to understand that fat storage is just the beginning.

The real damage begins when the liver responds to this strain. Fat accumulates in the liver, but the liver doesn’t just sit there inactive. Fat-rich liver cells undergo metabolic stress, triggering a series of inflammatory responses. This transition from simple fat accumulation (steatosis) to inflammation (steatohepatitis) represents a critical turning point in the disease process.

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Several mechanisms are involved in this inflammatory response.

1. Effects of Toxic Fats: When liver cells become overloaded with certain types of fats, especially saturated fats produced by the liver’s own lipogenesis, these fats can directly damage cell structures, much like trying to store cooking oil in a paper bag.
2. Oxidative stress: Fat-rich liver cells produce more harmful reactive molecules (similar to those that cause metals to rust), damaging cellular components and triggering an inflammatory response.
3. Destruction of cell factories: Accumulation of fat disrupts the normal functioning of the protein-producing machinery in liver cells (called the endoplasmic reticulum), triggering a stress response that promotes inflammation.
4. Immune system activation: Various immune cells, including the liver’s resident defense cells, become activated in response to these stressors and release inflammatory signaling molecules throughout the liver.

This inflammatory environment is what distinguishes simple fatty liver from the more severe form of nonalcoholic steatohepatitis (NASH). Although the course of simple fatty liver is relatively benign, NASH significantly increases the risk of progression to scarring (fibrosis), severe scarring (cirrhosis), and even liver cancer. Importantly, this same inflammatory environment causes increased cardiovascular risk and helps explain why my brother-in-law, who had fatty liver disease, ultimately died from heart disease.

This risk is particularly acute for Indians, who appear to be particularly susceptible to fatty liver disease. Some studies suggest a prevalence of 30% to 40% in urban populations. The IT industry seems to be particularly affected. A study conducted by the University of Hyderabad in 2023 and 2024 found that an astonishing 84% of IT employees have fatty liver disease. This increased risk may be due to several factors.

1. “Lean fat” phenotype: As explained in the previous chapter, Indians tend to have higher body fat percentages than Westerners, and even if they have a low BMI, they tend to have more visceral fat. This can predispose you to insulin resistance and fat accumulation in your liver, even if you don’t look visibly overweight. This is an important point. If you are an Indian, you don’t have to be obese to get fatty liver disease.
2. genetic factors: Certain genetic variations that affect fat metabolism and insulin signaling are more common in South Asian populations and may increase susceptibility to liver fat accumulation.
3. meal pattern: Rapid nutritional changes in India have resulted in increased consumption of refined carbohydrates and processed foods while maintaining traditionally high carbohydrate intake patterns. This combination is especially problematic for liver health.
4. sedentary lifestyle: Reduced physical activity levels in urban India have further reduced insulin sensitivity, impairing the liver’s ability to process nutrients efficiently.

These factors help explain why seemingly healthy, non-obese Indians often receive the shocking diagnosis of fatty liver disease. Many patients tell me they are confused. ”But Karan, I don’t drink, I’m not overweight, and I eat home-cooked meals…” Now you understand why these factors alone cannot protect our genetics and environment. context.

This excerpt from “Sick Nation” by Karan Sarin is published with permission from Wyzr Content.