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Obesity is not only about body shape and appearance, but also closely related to cardiovascular diseases, hormone secretion abnormalities and other health problems. In other words, obesity causes both physical and psychological problems. With the development of society, obesity has become a public health problem. Given the public's high awareness of obesity, and the variety of opinions surrounding it, what is at stake?

Some people think that obesity is because the intake of food energy is higher than the energy required for daily activities; some people think that obesity depends mainly on heredity, and some people are naturally prone to gain weight; some people think that sugar is the direct energy source of the body, and if you reduce the sugar content in the diet, you can lose weight. So, what exactly is the correct statement?

A recent paper published in Obesity suggests fructose is the culprit.

Fructose inhibits mitochondrial activity, lowering ATP levels in cells, and prevents fat cells from breaking down fat to produce ATP to replenish ATP in cells, thus prompting us to eat more fatty foods. In other words, many of the claims about obesity are correct to some extent, sugar, fat are the cause of obesity.

Major hypotheses about obesity The pathogenesis of obesity remains controversial. Heredity is an important factor, but environmental factors such as certain cultures and eating habits also contribute to the rapid rise in obesity rates. Now, some of the leading hypotheses for obesity include the following.

1) Energy balance hypothesis: heat can neither be created nor destroyed. The energy consumed minus the energy consumed is the energy stored in the body, that is, the fat in the body.

2) Carbohydrate-insulin model: obesity is considered to be an energy metabolism problem. Some pathological factors (such as increased insulin secretion) cause fat cells to store too much energy abnormally, and the amount of energy-supplying substances in body fluids such as blood is reduced, which leads to increased hunger and the body tends to eat more food.

3) Protein lever hypothesis: It is believed that the purpose of food intake is not to obtain enough energy, but to ensure adequate protein intake. Therefore, if the dietary protein content is too low, the body has to eat more food to meet a certain protein intake, resulting in excessive total energy intake, which leads to overweight and obesity.

4) Seed oil hypothesis: It is believed that the increase of obesity rate is closely related to the increase of vegetable oil consumption (high content of polyunsaturated fatty acids such as linoleic acid).

Each hypothesis has its own support, and its role in driving obesity is controversial. In the new study, the scientists found that fructose plays an important role in the obesity mechanism, and if another dietary hypothesis, the fructose survival hypothesis, is used to explain the obesity mechanism, these assumptions are largely correct.

Fructose Survival Hypothesis Fructose is found in sugar and high fructose corn syrup and can also be produced in the body from carbohydrates (especially glucose).

Fructose is unique in that it inhibits mitochondrial function, reducing ATP levels in cells (the most direct source of energy for the body, carbohydrates, fats are metabolized to produce ATP to provide energy for the body), while preventing ATP from decomposing fat from entering cells. Low intracellular ATP levels lead to carbohydrate-dependent hunger, impaired satiety (because fructose increases leptin levels, too much leptin reduces brain sensitivity to leptin, resulting in leptin resistance) and metabolic effects (increased metabolism and heat production to maintain and maintain normal body temperature; at the same time, increased metabolism of sugar, fat, and protein), resulting in increased intake of high-fat foods.

This hypothesis emphasizes the unique role of carbohydrates in stimulating food intake, and fat as the main source of energy in cases of excessive fructose intake. Therefore, we can say that obesity is a condition of energy metabolism disorder, that is, in the case of increased total energy, available energy (ATP) is low, and energy that does not play a metabolic role will lead to weight gain.

Fructose puts people into 'hibernation mode' Fructose is what triggers our metabolism to go into a low-power mode and lose control of appetite, but high-fat foods are the main cause of weight gain.

Take hibernating animals, for example, scientists say. If we feel hungry and have insufficient energy available, we enter survival mode-the body gradually depletes its stores of glycogen and fat and tends to rebuild the immune system by replacing damaged and aging cells. At the same time, there are thoughts of foraging and eating. From the perspective of fructose-induced obesity, we can understand why bears eat fruit to prepare for winter. Fruit is a high-fructose food, fat is a backup energy substance, eating high-fructose food will prevent the release of stored energy in fat, so that bears can safely survive hibernation by slowly burning fat.

Human beings do not need hibernation, and in the current highly developed material civilization, we usually do not lack food, especially in economically developed areas. Thus, the personal impact of excessive fructose intake is an imbalance in the body's energy supply system and weight gain, and the social impact is an increase in obesity rates and the incidence of obesity-related diseases.

Fructose also has a good effect. We know that fructose plays such an important role in the body's energy supply system. From another perspective, maybe we can use fructose to play a huge medical role.

Studies have shown that high fructose intake can trigger liver and colorectal tumors or promote tumor development due to fructose's specific mechanism of action. At the same time, studies have also shown that fructose can help alleviate lung tumors (so there seems to be a scientific basis for "pear moistening lung").

Recently, an article published in Cell Metabolism also showed that fructose regulates fat cell metabolism and raises leptin levels, which can enhance the anti-tumor immune response of CD8-positive T cells. Similarly, this effect of fructose is also more obvious in lung cancer patients, but not in colorectal cancer patients, and under the same fructose intake conditions, colorectal cancer patients have lower leptin levels.

Although the antitumor effect of fructose depends on tumor type, this new immunotherapy idea has great potential as an adjuvant therapy for cancer clinical treatment.

References:

https://doi.org/10.1002/oby.23920

https://www.cell.com/cell-metabolism/fulltext/S1550-4131(23)00367-4

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