Research on obesity is confirming what scientists have known for years: persistent weight problems are strongly associated with the chronically elevated insulin levels associated with a high carb diet.

Over the past 40 years, as Americans have embraced the low fat, high carbohydrate diet, the number of people who are significantly overweight has increased sharply. In addition, the number of obese children and children developing diabetes has also risen.

Research on obesity has even become a global concern as other countries and cultures have adopted the standard high carbohydrate American diet.

What is Insulin’s Role?

Insulinâ€™s job in the body is to store fat for future use and prevent the body from utilizing that fat for energy.

Chronically high levels of insulin cause accelerated and often permanent fat storage, and eventually lead to a condition called insulin resistance.

Gary Taubes writes about the research on obesity done in the past 100 years, and the role of insulin and carbohydrates in fat storage in his book Good Calories, Bad Calories.

In the book, he discusses the research on obesity in specific relation to the idea of malfunctioning insulin levels as a major cause of obesity, rather than the mainstream belief that weight gain is caused by too many calories and not enough exercise.

How Insulin Affects Fat Storage

According to Taubes, research on obesity has found that fat metabolism and storage in the human body is extremely dependent upon the action of insulin, blood sugar (glucose) and a substance called alpha glycerol phosphate, more commonly known as glycerol 3-phosphate.

Fat in the body comes in two main forms:

Fatty acids, which are a free form of fat which circulates in the bloodstream as fuel and

Triglycerides, which are a stored form of fat locked in fat cells.

The fatty acids are made of molecules that are small enough to move through cell walls, and so this form of fat flows freely in and out of our fat cells.

Triglyceride fat molecules are much larger. They consist of three fatty acids linked together via a glycerol molecule. Triglycerides cannot move through cell walls, so they become “locked” within the fat cell, once stored inside. They can only be released if they are broken down into fatty acid form.

Fatty acids are always circulating in the bloodstream. Inside each fat cell, a cyclical process of changing “triglycerides to fatty acids to triglycerides” happens continuously, depending on the needs of the body.

The whole process is driven by the presence of insulin, glucose and glycerol 3-phosphate. Other hormones such as epinephrine, adiponectin, leptin, glucagon and growth hormone also play a part, but insulin will override these if it is present.

Fatty acids are stored in the fat cells in a more solid, locked triglyceride form when a substance called glycerol 3-phosphate is present.

Where does the glycerol 3-phosphate come from? It’s a product of carbohydrate metabolism. When carbohydrates are consumed, they are metabolized into simple sugar molecules which then flow into the bloodstream. The body responds by releasing insulin to move the sugar out of the bloodstream and into the cells.

Once insulin has moved the blood sugar into the cells, the cells use it as a fuel for the cellular activity. When the sugar is burned for fuel, glycerol 3-phosphate is created.

Because the glycerol 3-phosphate is now present, any fatty acids flowing into the fat cell are converted into triglyceride form and stored via a process called esterification.

So, fat storage follows a simple process:

When blood sugar and insulin are low, stored triglycerides are converted into fatty acids which then flow from the fat cells as needed for fuel.

When blood sugar and insulin levels are high, insulin moves the glucose into the cells, where it is burned for fuel, creating glycerol 3-phosphate. When glycerol 3-phosphate is present in the cell, fatty acids are converted into triglycerides and stored.

More importantly, the continual presence of insulin, glucose and glycerol 3-phosphate ensures that fat is stored permanently in triglyceride form within the cells.

So the bottom line is that the body stores fat when sugar (in the form of carbohydrate) is available as an alternative fuel.

The more carbohydrates consumed => the more insulin in the blood moving glucose into the cells => the more glycerol 3-phosphate is available => the more fat is stored.

If your goal is to lose fat, you have to reverse this process:

To reduce the amount of fat stored in your fat cells as the permanent triglyceride form, you must reduce the amount of ingested carbohydrates. This, in turn, reduces the amount of circulating glucose and resting insulin levels, which then reduces the amount of glucose and glycerol 3-phosphate in the cells. Once insulin levels fall to normal levels, and carbs are limited, the triglycerides are then broken down into fatty acid form so it can flow out of the fat cell, and into the bloodstream to be used as fuel.

You cannot store fat in the fat cells without the presence of insulin, glucose and glycerol 3-phosphate.

This is why people can eat many more calories on a low carb diet and still lose weight.

This process and other research on obesity explain why the marker of Type I diabetic diagnosis is the rapid loss of weight.

Type I Diabetics don’t have enough insulin circulating in the blood to move glucose into the cells where it can be burned to create alpha glycerol phosphate. Without insulin, sugar can’t be moved into the cells, and glycerol 3-phosphate can’t be made, no fat can be stored in triglyceride form.

Other Research on Obesity

Some of the newest research on obesity involves the following factors:

Leptin: a hormone produced by adipose (fat) tissue which regulates appetite and weight gain.

Adiponectin: a hormone produced in abundance by fat tissue. It is associated with glucose and fatty acid metabolism and is a factor in increasing insulin sensitivity of the cells.

Irvingia gabonensis: an extract of the African mango tree which has been shown to promote weight loss.

Resources for Further Reading on the Research on Obesity