english

Our enemy obesity

 

Despite the recent popularization of so-called extra size models, still one of the most common New Year’s decisions is losing weight. As much as we give our best, some people just can not lose their weight.

For the survival of man, a constant supply of energy is needed. Since in the past man did not have the luxury of regular meals (and needs a constant supply of energy), the organism had to adapt to this terms by storing energy in the form of fat, from which it can easily be released (our organism is a great pessimist, always ready for the worst). However, today when most people are surrounded by easily accessible (often high-calorie) food, combined with poor physical activity, we get an increasing medical problem – obesity.

 

 

 

The amount of energy, or its balance in the body, is regulated through food intake and energy consumption. When the brain sends the signal that we are hungry, it means that the current amount of energy reserve in the fat tissue is not enough. The fat tissue informs the brain about this by producing leptin. Leptin in the brain can act in 2 ways: if in small quantities, a center for hunger triggers and reduces energy consumption; if it is present in a larger volume, a center for fullness is activated and energy consumption is increased. Energy is consumed through basic metabolic reactions necessary for survival (breathing, heart beating, enzyme activity and hormone production), physical activity and heat generation. Physical activity increases the speed of metabolic reactions (accelerates metabolism).

Insulin may also stimulate the production of the aforementioned leptin and thereby affect the feeling of fullness, but insulin can also increase hunger if a person has low blood sugar.

It would be logical that obese people had less leptin in the blood, which would explain why they eat more food and store more energy. But the situation is quite the opposite – obese people have higher blood levels of leptin. Explanation? They are resistant to leptin, meaning their brain does not respond adequately to leptin. In addition, it has been shown that  fatty tissue of obese people has more substances whose concentration increases during inflammation (so-called cytokines), and that muscle and fatty tissue sensitivity to insulin is reduced (this means that these people are at a very high risk of getting diabetes).

Inheritance is responsible 30-40% for obesity, because some people simply have a genetically greater affinity to fat deposits and reduced energy consumption.

The type of food also has great significance. Fat has more calories, and it is possible that the mechanism for regulating appetite responds slower on fat than sugars and proteins, so that the person will eat more fatty foods before they get the signal they are full.

The common problem is gaining weight after you lose some. The reason is the following: Suppose you have reduced your calorie intake while being on a diet, which means you have less energy intake than the amount you spent, so your energy balance is negative. As a result, the rate of metabolism decreased, and thus reduced energy consumption (just to make it clear: the amount of energy spent  during diet is still higher than its intake, but consumption decreased compared to pre-diet period). Thus, a person who has been overweight and now has normal weight needs less calories to maintain normal weight than a person who has never been overweight. The point is, once you go on a diet, you need to stay on a diet, almost your whole life to maintain your normal weight. Once a diet, always a diet!

 

Of course, psychological, cultural and social factors play a major role in the emergence of obesity. Unfortunately, this means that we can not go for: “I’m sorry, I’m resistant to leptin” and eat the whole cake, but we need to ask ourselves why we want to eat the whole cake.

 

 

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