What Is The Fate Of Excess Carbohydrate? Does It Turn Into Fat?

Does eating carbohydrate, starch, make us fat? The short answer is “No.” The caveat is “No, as long as the diet is not also high in fat.”

The carbohydrate we eat has many fates. One fate, after it’s broken down into glucose, is energy production. That’s its primary fate. Its next fate is the replenishment of glycogen. (Glycogen is a form of energy storage. It’s made up of many units of glucose strung together.) A pound of glycogen stores about 1800 calories. We can store several pounds of glycogen in the body – in liver, muscle, even fat cells store glycogen. We can store A LOT of calories from the carb we eat as glycogen without turning it into fat. Fat production does occur, but it does not rank high in the body’s use of glucose.*

In humans there is little lipogenesis [fat production] from glucose under normal conditions.

What is the fate then of excess glucose?

1. It warms the body:

Thermogenesis [heat production] can help eliminate a sizeable part of the excess unused dietary glucose.”

2. It can be consumed by gut bacteria:

An undetermined part of the excess body glucose may find its way into the intestinal lumen [glucose freely diffuses across the intestinal wall, both ways], where it may be taken up and metabolized by the microorganisms.

3. It can be lost in urine: From blood, glucose travels to kidneys where it’s excreted. At one time, people tested for diabetes by tasting urine for sweetness.

People known as “water tasters” diagnosed diabetes by tasting the urine of people suspected to have it. If urine tasted sweet, diabetes was diagnosed. To acknowledge this feature, in 1675 the word “mellitus,” meaning honey, was added to the name “diabetes,” meaning siphon.

4. It can be used for fat production. But that has limits:

Excess glucose has difficulty entering cells (for fat production) if the cell has already satisfied its glucose needs. How does the cell close the door to too much glucose, which can damage the cell? By becoming resistant to insulin, a hormone which opens the door. High-caloric/high dietary-fat environments cause cells to become insulin resistant. Blood glucose then rises. That causes insulin to rise even more, leading to a cascade of largely undesirable effects. Insulin is an anabolic hormone and supports lipogenesis/fat production – but the preferred substrate or building block for fat production is fatty acids, not glucose:

Brown adipose [fat] tissue (BAT) enhanced consumption of glucose may represent a quantitatively significant possibility for rodents, but it is doubtful that in humans, with a limited BAT presence, it may represent a significant dent in the pool of excess circulating glucose, especially when BAT preferred substrate is, again, lipid.

A number of tissues, such as white adipose tissue (WAT), however, develop the ability to deactivate a significant proportion of the insulin carried by the blood, a mechanism that protects the tissues themselves of being force-fed an unwanted and not metabolizable [because of saturation of normal pathways] load of glucose.

A high-caloric diet where fat calories are in abundance can lead to chronic insulin resistance, diabetes, inflammation, high blood cholesterol, fatty liver … the very definition of the metabolic syndrome.

People do not get fat eating lots of carbohydrate. Look at the rice diet, or the potato diet. In fact, people tend to lose weight … as long as they are not pouring oil on salads and pasta or melting cheese over vegetables or eating lots of just about any animal food which contains most of the saturated fat and cholesterol in the human diet.

Whole populations have survived and thrived on diets that received most of their calories from carbohydrates – rice, potatoes, corn, wheat, barley. And they did not not have the obesity problems we have today.

Dr. McDougall says, “The fat you eat is the fat you wear.” He’s right. (This article said it more scientifically, “Dietary lipids favor their metabolic processing.”)

* Utilization Of Dietary Glucose In The Metabolic Syndrome, Nutrition and Metabolism, 2011

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