The Link Between Insulin Resistance and Chronic Diseases: What You Need to Know

causes a rise in blood glucose levels. Insulin resistance, a condition where cells become resistant to the effects of insulin, leads to an excess of glucose in the bloodstream. This video explains that insulin resistance is not solely caused by insulin deficiency, but rather by an overflow of glucose in the cells. This excess glucose prevents the cell from taking in any more glucose, despite high insulin levels. The result is a buildup of glucose in the blood, eventually leading to the diagnosis of type 2 diabetes. Insulin resistance can occur for years before diabetes is diagnosed, and during this time, individuals may already be suffering from chronic diseases such as heart disease and kidney damage. It is crucial to detect and address insulin resistance early on to prevent further complications.

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How does this happen?

Key Insights:

  • Insulin resistance occurs when the body’s cells are resistant to the effects of insulin, which causes high blood glucose levels.
  • In type 1 diabetes, the body does not produce insulin, resulting in the inability of glucose to enter the cells.
  • In type 2 diabetes, the cells have too much glucose, making it difficult for insulin to move glucose into the cells.
  • The traditional understanding of type 2 diabetes assumes that high blood glucose causes all the problems, but this oversimplification overlooks the overflowing of glucose within cells.
  • Insulin resistance can be compared to a restaurant with a door that is open but the restaurant already being full, so more people can’t be let in despite the open door.
  • The problem of insulin resistance lies in the excess glucose in the body, not insulin itself.
  • Before the diagnosis of type 2 diabetes, individuals may experience a long period of insulin resistance, which can lead to chronic diseases such as diabetic kidney disease and heart disease.
  • High insulin levels contribute to heart disease by causing narrowing and hardening of the arteries, independent of cholesterol levels.
  • The chronic effects of insulin resistance may occur before the development of type 2 diabetes and can impact individuals regardless of their body weight.
  • The risk of heart disease and stroke can exist in the period of insulin resistance before the onset of type 2 diabetes.
  • Insulin resistance can occur in individuals of normal weight, emphasizing the need to consider factors beyond body mass index in assessing health.


Insulin resistance is a term used when the blood glucose level is high, and the body produces more insulin to allow glucose to enter the cells for energy. It is believed that insulin resistance occurs when there is plenty of glucose in the blood but it is not entering the cells effectively, indicating resistance to the effects of insulin. In type 1 diabetes, there is no insulin, so glucose cannot enter the cells. In type 2 diabetes, there is plenty of insulin, but for some reason, the insulin is not opening up the cells to allow glucose entry.

One way to understand this is to think about a restaurant. Normally, when the doors are open, people enter the restaurant. But if the doors are closed, the people stay outside. This is similar to type 1 diabetes where there is no insulin to open the doors. In type 2 diabetes, it is like the doors are wide open, but the restaurant is already full, so no more people can enter.

However, there is a flaw in this understanding. If the cells are not receiving glucose and are empty, people should be thin and have small livers. But in reality, people with type 2 diabetes are often overweight with fatty livers, indicating that their cells are not starving but overflowing.

It suggests that the cells have an excess of glucose, making it difficult for more glucose to enter despite sufficient insulin. The problem lies in the excess glucose rather than the effectiveness of insulin. The initial response is for the body to produce more insulin to remove the excess glucose from the bloodstream. Eventually, the system breaks down when insulin levels dip, leading to high blood glucose levels and the diagnosis of type 2 diabetes.

During the early stages, the body can compensate by producing more insulin to forcefully push glucose into the cells. The result is a cell that is filled with glucose but requires extra insulin to achieve this. This leads to a condition called hyperinsulinemia, characterized by high insulin levels in the blood even when glucose levels are normal. Hyperinsulinemia occurs much earlier than the increase in blood glucose levels.

This compensatory mechanism can only work for a limited time. Eventually, the cells reach their limit, and no amount of insulin can push more glucose into them. At this point, glucose remains in the blood, and type 2 diabetes is diagnosed. However, the underlying process has been ongoing for a long time before diagnosis.

Doctors primarily focus on measuring blood glucose levels to diagnose type 2 diabetes, which is a late-stage indicator. This approach is based on an outdated concept that high blood glucose is the main problem. However, the real issue lies in the overflowing cells with excess glucose. These problems are often overlooked until diagnosis, leading to missed opportunities for early intervention.

To understand where an individual falls along the spectrum of insulin resistance without diabetes, various indicators can be used. These include the presence of metabolic syndrome, characterized by high blood pressure, high triglycerides, low HDL cholesterol, abdominal obesity, and insulin resistance. Abdominal circumference can be a proxy for body fat since fat tends to accumulate in the abdominal area in metabolic syndrome. Additionally, fasting insulin levels can provide clues, although they may vary throughout the day.

Insulin resistance can contribute to the development of chronic diseases, including heart disease, stroke, and kidney disease, long before the diagnosis of type 2 diabetes. Insulin has proatherogenic effects, causing arterial wall damage and narrowing, leading to cardiovascular complications. It is well-known that insulin plays a significant role in the development of atherosclerosis, which is the hardening and narrowing of the arteries. This suggests that insulin, rather than cholesterol, is a major factor in cardiovascular disease. Insulin resistance increases the risk of these diseases, even before diabetes is diagnosed.

The period of insulin resistance before the onset of type 2 diabetes can last for many years, allowing chronic diseases to develop. Individuals may experience chronic kidney disease associated with metabolic syndrome, even without diabetes. The damage caused by hyperinsulinemia starts before the diagnosis, leading to early signs such as protein in the urine.

While some chronic diseases may occur before diabetes, the risk and severity can vary among individuals. Factors such as age, sex, genetics, exercise, smoking, and cholesterol levels can also contribute to heart disease. However, diabetes remains a significant contributor to cardiovascular complications, and its reversal is crucial as it is a reversible risk factor. Reversing type 2 diabetes through dietary changes, weight loss, and proper management can mitigate the risk of chronic diseases.

It is important to note that insulin resistance can occur even in individuals who appear skinny or have a normal body mass index (BMI). BMI is not always an accurate reflection of body fat versus lean mass. Some people with normal weight based on BMI may still develop type 2 diabetes due to insulin resistance, emphasizing the need for comprehensive evaluation beyond weight alone.

In conclusion, understanding insulin resistance and its impact on health is crucial for early detection and intervention. Insulin plays a significant role in the development of chronic diseases, including heart disease and kidney disease, even before the diagnosis of type 2 diabetes. Addressing insulin resistance through lifestyle changes can significantly reduce the risk of these complications and improve overall health.