Fructose affects obesity more than glucose

Fructose can affect the formation of obesity more than glucose. From a nutritional point of view, both fructose and glucose contain no essential nutrients. The properties of the two are similar, but fructose is more harmful to human health than glucose because the body has a unique way of fructose metabolism.

Every cell in the body can use glucose to produce energy, but fructose must be metabolized through the liver. Excess glucose can be dispersed throughout the body as energy, and fructose is aimed at the liver like a missile.

When we eat a lot of glucose, such as starch, these sugars will circulate to each cell and help disperse the sugar load.

Cells outside the liver can metabolize 80% of the body’s intake of glucose. During the meal, the heart, lungs, muscles, brain, and kidneys can absorb this “buffet-style” glucose meal, leaving 20% ​​of the remaining liver to digest and convert to glycogen storage.

In other words, when we eat large amounts of fructose, they only flush to the liver because no cells can use or metabolize them. Think about the significance of this for a normal person weighing about 77 kilograms. Sucrose provides equal amounts of glucose and fructose.


While 77 kg of body metabolize glucose, only about 2 kg of liver must bravely metabolize all fructose.

And the liver will work hard to metabolize fructose to glucose, lactose and glycogen, so the more you eat, the more metabolism you have. There is also a refining process that removes natural protein, fiber, and fat from carbohydrates. The removed ingredients also take away a sense of satiety.

For example, a 1,000-calorie baked potato will make you burp, but the same 1,000-calorie sugary coke won’t, although both are carbohydrates, but the former is raw and the latter is highly processed.

In fact, we digest digested carbohydrates such as high-fructose corn syrup faster because we will not feel full, we will eat more, and blood sugar will rise. When the glycogen stores are fully loaded, the process of lipid neogenesis (DNL) converts the excess fructose directly to hepatic fat.

Excessive intake of fructose increases the lipid production (DNL) by a factor of 5 and replaces glucose with fructose of the same calories, which increases liver fat by 38% in just 8 days. This fatty liver is crucial in the development of insulin resistance.

Among all carbohydrates, the ability of fructose to trigger fatty liver is unique. In addition, this malignant effect from fructose can be destroyed without the aid of hyperglycemia or high insulin concentrations. The problem of fructose causing fatty liver is as fast and inevitable as a bullet train, and it will stimulate the increasing of insulin resistance.

Since fatty liver and insulin resistance due to it are the key to hyperinsulinemia and obesity, this means that fructose is far more dangerous than glucose.

It is conservatively estimated that for an average person of 77 kilograms, the risk of fatty liver caused by fructose is approximately 34 times, which in turn leads to obesity and insulin resistance. This is very similar to how the body metabolizes ethanol (alcohol). Once ingested, the tissue can only metabolize 20% of the alcohol, and the remaining 80% go directly to the liver.

The liver metabolizes alcohol to acetaldehyde, which in turn promotes lipidic neogenesis (DNL), so alcohol and fructose are as easy to form as liver fat. This also explains the role of alcohol intake in triggering fatty liver disease.

As early as 1980, it has been known that experiments have shown that excessive intake of fructose stimulates insulin resistance. Healthy subjects consume more than 1,000 calories of fructose per day and their insulin sensitivity deteriorates by 25% after only 7 days. In contrast, subjects who consumed glucose in excess did not experience any similar deterioration.

A 2009 study reinforced the argument that fructose is an easy cause of insulin resistance in healthy subjects.

Subjects drink a beverage that is instant, has a variety of fruit tastes, and accounts for 25% of the total daily calories. This number may seem remote, but many people do indeed consume such a high percentage of sugar in their diet.

The fructose group (but not the glucose group) increases their insulin resistance so that they are clinically classified as pre-diabetic, and this development requires only 8 weeks of excessive fructose uptake.

It is worth noting that over 1 week of fructose intake can cause insulin resistance. It only takes 8 weeks to make pre-diabetes raging. What happens after decades of high fructose ingestion?

The answer is diabetes, which is exactly what we are currently facing.

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