Can't help eating? It's not your fault! Maybe there's something wrong with your body.

Can't help eating? It's not your fault! Maybe there's something wrong with your body.

With the arrival of winter, the weather is getting colder, and many people have entered a rhythm where they always want to eat, always eat, and simply cannot stop.

All kinds of steaming delicacies tempt us, and coupled with the fact that we wear more clothes to hide our fat, the result is that we eat more and more, and the more we eat, the fatter we get, and the fatter we get, the more we want to eat. So, how can we break this "eat more and more" curse?

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Always "can't control your mouth"

Maybe it's not that you don't have enough willpower.

If we want to “control our mouths”, we must first know what makes us unable to control our mouths.

Previously, people believed that the control of eating response was mainly dominated by " orexigenic neurons (AGRP/NPY)" and " orexigenic neurons (POMC)" in the arcuate nucleus of the hypothalamus. The former stimulated and promoted appetite, while the latter inhibited appetite.

Both types of neurons are regulated by "leptin", a hormone secreted by adipose tissue. When leptin is secreted in large quantities, the action of "orexigenic neurons" is inhibited, while "orexigenic neurons" are activated, thereby stopping eating behavior. On the contrary, when leptin is secreted in small quantities, eating behavior is strengthened and promoted. Unfortunately, "orexigenic neurons" are far weaker than "orexigenic neurons" in terms of both the speed and strength of regulating eating behavior.

Recently, an article published in the world's top journal Nature pointed out that researchers have discovered a new neuron BNC2 that can participate in food intake regulation in animal experiments. This neuron is located in the arcuate nucleus of the hypothalamus. Its activation can inhibit "food-promoting neurons" and quickly induce the body to produce a sense of satiety, which plays a role in suppressing appetite and reducing feeding response.

It seems that BNC2 greatly makes up for the defects of "anxiety suppressing neurons" in regulating eating behavior. At the same time, it can enhance insulin sensitivity after being activated, which is also helpful in regulating blood sugar levels. But why do we still "eat more and more and lose control of our appetite" from time to time?

Scientists have found that in many cases, even if the leptin level in the blood is high, eating behavior is still not inhibited, and both experimental animals and humans still feel "hungry" and want to eat. This is because of the existence of "leptin resistance": that is, the leptin receptors in the arcuate nucleus of the hypothalamus of animals or humans have become weaker and slower to respond to leptin stimulation . Although BNC2 is powerful, it cannot solve the problem of leptin resistance. Once the leptin receptors on the arcuate nucleus are not working, increased eating and obesity will still occur.

This means that sometimes we can’t stop eating, not because of a lack of willpower, but because our brain is damaged and can’t help us regulate and control our eating behavior.

What causes "leptin resistance"

What makes us unable to stop eating?

In daily life, understanding the causes that may cause "leptin resistance" can help us identify our inappropriate eating and living habits that are quietly controlling our eating behavior.

1

Overeating

Studies have found that repeated overeating can damage the arcuate nucleus of the brain and increase the chances of obesity . Does it sound like a vicious cycle?

The more you eat, especially the more saturated fat you take in, the more likely you are to develop leptin resistance. Once leptin resistance occurs, more leptin is needed to send the signal "I'm full, it's time to stop eating" to the brain. Leptin is secreted by fat, so more fat is needed. If you want to store more fat, you need to eat more...

Doesn’t this form a perfect closed loop of “the more you eat, the more you want to eat”? No wonder we find that the fatter we get, the harder it is to control our appetite.

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2

Sleeping too late

Many studies have found that insufficient melatonin secretion caused by sleeping too late or circadian rhythm disruption may affect leptin signaling, causing experimental animals to show long-term leptin resistance.

Well, there is one more charge for sleeping too late. In addition to making our skin look bad and making us lack energy, it will also increase our appetite due to leptin resistance, making us inevitably gain weight.

3

Diets high in sugar, fat, and salt

Researchers have found that increased levels of inflammation in the body increase the risk of leptin resistance. In some animal experiments, a high-fat diet can cause an inflammatory response in the hypothalamus of mice, which in turn leads to leptin resistance. Other studies have found that C-reactive protein, which appears during the acute phase of inflammation, has been shown to inhibit the expression of leptin receptor signals, leading to a rapid increase in leptin resistance, body weight, and food intake in mice. A high-sugar diet has also long been shown to increase the body's level of inflammation.

Another thing that cannot be ignored is a high-salt diet, which is not only likely to cause high blood pressure and cardiovascular and cerebrovascular diseases, but may also lead to leptin resistance and insulin resistance. Experiments have confirmed that reducing salt intake is beneficial for protecting leptin sensitivity.

In simple terms, if there are too many high-fat, high-sugar and high-salt foods in the diet, it may cause leptin resistance due to inflammatory response, leading to more eating. You see, the benefits of a light diet are increased again.

Although there are more reasons that lead to leptin resistance than mentioned above, these three aspects are relatively easy to improve in our daily life.

Want to overcome "leptin resistance"

This is more effective

Fortunately, "leptin resistance" is not completely irreversible. As long as we work hard in the following aspects, we can still alleviate the "leptin resistance" condition.

1

Consciously control the amount and frequency of food intake

Especially in the face of the high-fat, high-salt, and high-sugar diets common in New Year gatherings, we must consciously control the amount of food we eat and reduce the frequency of snacking. Reducing the intake of calories and fat can reduce damage to the arcuate nucleus of the brain and gradually break the terrible vicious cycle.

2

Exercise is essential

Studies have shown that regular exercise can not only reduce excessive leptin levels in the blood, but also stimulate the sensitivity of the arcuate nucleus to leptin. This effect is more significant when combined with diet control.

Some researchers have suggested that in order to improve leptin resistance, long-term, high-intensity exercise is not recommended. Walking and swimming are more recommended. This can be used as a reference for everyone.

3

Please get enough sleep

Sufficient sleep that is in line with the natural circadian rhythm can ensure adequate melatonin secretion and improve leptin resistance caused by melatonin deficiency.

In fact, for us, a more effective way is to take at least one hour during the day to walk outdoors and bask in the sun, and turn off the mobile phone early every night to reduce the stimulation of blue light from the mobile phone screen, so that the body can gradually return to a healthier rhythm of work and rest.

4

Eat more natural, light, and varied foods

According to the recommendations of the "Dietary Guidelines for Chinese Residents", we should eat more natural, light and diverse foods.

For example, you can add more fresh fruits and vegetables, especially dark green vegetables and dark berries such as blueberries, strawberries, and grapes; whole grains rich in dietary fiber, green tea, and soy; deep-sea fish rich in polyunsaturated fatty acids, etc. into your daily diet. This is not only to meet nutritional needs, but also because these foods are not likely to cause leptin resistance.

Copyright images in the gallery. Reprinting and using them may lead to copyright disputes.

Desserts made from refined grains, cakes, various high-sugar snacks, processed meats, alcoholic beverages, high-fat fried and grilled foods, and other heavy-tasting, deeply processed foods can easily cause leptin resistance, making us want to eat more and can't stop. We should try to eat less or no food at all.

We always say that losing weight is easier said than done. In fact, if we can break down the goals of improving leptin resistance and controlling appetite into small actions, even if we only do one of them every day, it will be a positive feedback to the body. The body gives us the opportunity to "reform ourselves", and we must actively seize it.

References

[1]Friedman, JM Leptin and the endocrine control of energy balance. Nat. Metab. 1, 754–764 (2019).

[2]Xu, J. et al. Genetic identification of leptin neural circuits in energy and glucose homeostases. Nature 556, 505–509 (2018).

[3]Tan, HL, Yin, L., Tan, Y. et al. Leptin-activated hypothalamic BNC2 neurons acutely suppress food intake. Nature (2024).

[4]Caro JF, Kolaczynski JW, Nyce MR, et al. Decreased cerebrospinal-fluid/serum leptin ratio in obesity: a possible mechanism for leptin resistance[J]. Lancet, 1996, 348(9021): 159–161.

[5] Ding Wenling, Liu Changyun, Song Maoyuan, et al. Effects of leptin resistance and its receptor gene mutation on lipid metabolism in children with simple obesity[J]. Chinese Journal of Practical Pediatrics, 2012, 27(7): 492–494.

[6] EA Schur, SJ Melhorn, S.-K. Oh, JM Lacy, KE Berkseth, SJ Guyenet, et al., Radiologic Evidence That Hypothalamic Gliosis Is Associated with Obesity and Insulin Resistance in Humans, Obesity (Silver Spring, MD) 23, no. 11 (November 2015): 2142-48.

Front Endocrinol (Lausanne). 2018 Mar 27;9:122.

[8]Buonfiglio D, Tchio C, Furigo I, Donato J Jr, Baba K, Cipolla-Neto J, Tosini G. Removing melatonin receptor type 1 signaling leads to selective leptin resistance in the arcuate nucleus. J Pineal Res. 2019 Sep;67(2):e12580.

[9]Carraro RS, Souza GF, Solon C, Razolli DS, Chausse B, Barbizan R, Victorio SC, Velloso LA. Hypothalamic mitochondrial abnormalities occur downstream of inflammation in diet-induced obesity. Mol Cell Endocrinol. 2018 Jan 15;460:238-245.

[10]Mendes NF, Gaspar JM, Lima-Júnior JC, Donato J Jr, Velloso LA, Araújo EP. TGF-β1 down-regulation in the mediobasal hypothalamus attenuates hypothalamic inflammation and protects against diet-induced obesity. Metabolism. 2018 Aug;85:171-182.

[11] Lanaspa MA, Kuwabara M, Andres-Hernando A, Li N, Cicerchi C, Jensen T, Orlicky DJ, Roncal-Jimenez CA, Ishimoto T, Nakagawa T, Rodriguez-Iturbe B, MacLean PS, Johnson RJ. High salt intake causes leptin resistance and obesity in mice by stimulating endogenous fructose production and metabolism. Proc Natl Acad Sci US A. 2018 Mar 20;115(12):3138-3143.

[12] Peng Jin, Yang Yajun, Wang Xiaohui. Research progress on exercise improving leptin resistance in obesity and its mechanism[J]. Progress in Biochemistry and Biophysics, 2021, 48(9): 1023-1030.

Planning and production

Author: Wang Lu, registered dietitian

Review | Ruan Guangfeng, Deputy Director of Kexin Food and Health Information Exchange Center

Zhao Wei, Chief Physician, Department of Neurology, Tianjin Teda Hospital

Planning丨Wang Mengru

Editor: Wang Mengru

Proofread by Xu Lailinlin

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