Medicosnext
Prof. Dr. Sanjaya Kumar Shrestha
For most of the human history, we were not office-workers, restaurant-goers or snack-eaters.
We were hunters and gatherers. Food was uncertain. Hunting could fail. Climate could change. Famine was more common than feast. Our bodies therefore evolved to survive long periods without food. We mainly ate animal protein, animal fat, and only small, seasonal amounts of carbohydrates from naturally growing plants. Yet our cells, especially the brain, needs glucose to function. So human metabolism evolved to make glucose internally from protein and fat and to store surplus energy safely as body fat. This fat storage was not a mistake. It was a survival tool.
Farming changed our food – but not our biology
When humans started farming, carbohydrate intake increased. Grains and plant foods became a major part of the diet. But even after agriculture hunger was still common, physical activity remained high, and food availability was still unstable. Our metabolic system could still cope.
The real turning point: refined sugar
The major disruption came only in the last 150–200 years. For the first time in human history refined sugar, refined flour, and highly processed foods became cheap, abundant and continuously available. We felt happy eating sugar and sugary products. Only recently, we realized that sugar stimulates the release of dopamine in the brain the same “reward” pathway that reinforces pleasure and craving. This is one reason why sugary foods are unusually addictive.
Historically, sugar was even considered a luxury and a symbol of social status. With large-scale cultivation of sugar-producing plants, sugarcane, it became a daily commodity. Now, feasts have become more frequent than famine.
The fat that once saved us
Our bodies respond to frequent carbohydrate and sugar intake by storing energy as fat. A special type of fat accumulates inside the abdomen, around internal organs. This is called visceral fat, often described as “belly fat”. In ancient environments, this fat provided fast energy during long fasting, and supported survival during famine. But there is an important biological rule – visceral fat was designed to be filled and emptied repeatedly. Today, it is filled continuously, and rarely emptied.
Why long-stored visceral fat becomes inflammatory
When visceral fat cells stays in place for a long period of time their blood and oxygen supply becomes relatively insufficient, their internal machinery becomes overloaded, and their mitochondria become stressed. A chronically overfilled fat cell behaves like an injured cell. It begins to release inflammatory substances called cytokines. Immune cells enter the fat tissue, trying to repair the stressed cells. Therefore, visceral fat gradually becomes an inflammatory organ, not just a storage tissue. This is one of the earliest and silent sources of inflammation in the body.
How belly fat leads to insulin resistance
Enlarged visceral fat releases excessive fatty acids directly into the blood. These fatty acids enter the liver and skeletal muscle. Inside these organs, excess fat interferes with normal insulin signaling. At the same time, inflammatory signals released from visceral fat further block insulin action. The result is insulin resistance. Insulin is still produced, but the body does not respond to it properly.
Why insulin resistance silently raises insulin
To keep blood glucose level normal, the pancreas compensates by producing more and more insulin. So in early metabolic disease blood sugar may still look normal, but insulin is already high. This stage is often completely missed in routine check-ups unless your doctor is aware of this mechanism and advises you to check for it.
How high sugar directly inflames blood vessels
High and frequent sugar spikes in blood result in a chemical reaction called non-enzymatic glycation which means glucose molecules are automatically attached to protein molecules. Important proteins that become glycated are albumin and lipoproteins that carry cholesterol in the blood, and structural proteins of the blood vessel lining. These modified proteins are called advanced glycation end-products (AGE). AGEs activate specific receptors known as receptors for advanced glycation end-products (RAGE) on blood vessel cells and immune cells. This AGE-RAGE reaction triggers continuous inflammatory signaling inside the vascular wall.
Two different inflammations working together
So, in modern lifestyle, two powerful inflammatory processes act at the same time:
- Visceral fat inflammation
Driven by fat-cell stress and insulin resistance. - Sugar-driven vascular inflammation
Driven by glycation and AGE-RAGE reaction.
Together, they create a long-lasting inflammatory environment inside blood vessel wall that leads to scarring known as atherosclerosis. This process is one of the major drivers of damage to the inner lining of the blood vessels, the endothelium. When these scars rupture blood clot forms and blocks the blood supply. If it occurs in the heart it results in heart attack and if it happens in the brain it results in stroke or paralysis. According to the World Health Organization, these cardiovascular diseases are now the leading cause of death worldwide, approximately 19 million deaths every year.
What is insulin resistance?
Insulin resistance means your body needs more and more insulin to do the same job. It is not a disease of glucose alone. It is a disease of metabolism, inflammation and energy overload.
What HbA1c really tells you?
HbA1c measures how much of your haemoglobin has been exposed to glucose over the past 2–3 months. It reflects how often your blood sugar rises, and how high those rises are. HbA1c is therefore a marker of chronic sugar exposure and glycation stress.
What HOMA-IR tells you and why it matters
HOMA-IR is calculated from fasting glucose and fasting insulin. It reflects how much insulin your body must produce just to maintain fasting glucose. A high HOMA-IR usually means insulin resistance is already present, and compensatory hyperinsulinaemia is already operating. In simple terms HbA1c reflects sugar-related damage. HOMA-IR reflects insulin-resistance-driven metabolic stress. Both are closely linked to inflammation and future cardiovascular risk.
Why these numbers quietly reflect your future health
Long before diabetes appears, the body may already have expanding visceral fat, rising insulin levels, low-grade inflammation, and endothelial dysfunction. This is the stage where future heart attacks and strokes are silently programmed.
A practical message for the public
If you are overweight, especially have an increased abdominal fat, do not rely only on fasting blood sugar or after-meal blood sugar. You should also know your HbA1c and your HOMA-IR (calculated from fasting glucose and fasting insulin). Even when HbA1c is still normal, a high HOMA-IR may already indicate ongoing inflammation, insulin resistance, and early metabolic injury.
Final thought
The ancient survival-oriented metabolism is now exposed to continuous sugar and constant food availability. The fat that once protected us during famine in a modern environment become a silent inflammatory organ. Let us try and detect this process early, before diabetes, before heart attack, before stroke, we still have the chance to reverse it.
Your belly fat and your insulin resistance are not just cosmetic issues. Remember, they are biological signals about your future health and longevity.
