Why are we hungry

How hunger and satiety work

It used to be thought that as soon as the stomach was empty, it began to contract and trigger the feeling of hunger. Today we know that things are more complicated: When we get hungry, not only has something to do with our stomach, but also with our cell metabolism and with signals from our brain. However, it is only in the beginning that we know exactly how these work.

It is known that hunger and saturation mediated by a specific region in the brain called the hypothalamus. Two centers work here, the hunger center and the satiety center. These centers release hormones into the blood that cause either food intake or a stop to eat: The hunger center releases the "hunger hormones" neuropeptide Y, agouti related peptides (AGRP) and melanin concentrating hormones (MCH) as well as cannabis-like hormones (endocannaboids). The satiety center works primarily with the "satiety hormones" propiomelanocortin (Alpha-MSH), CART and serotonin. How hard the hunger center and the satiety center work depends on signals from the body: a falling blood sugar level indicates hunger, while the increased amount of insulin released when the blood sugar level is high activates the satiety center. Certain amino acids (such as tryptophan) and fatty acids from food also send signals to the hunger and satiety center.

Signals from the gastrointestinal tract also play a role: through the Stretching of the stomach certain hormones are released on the stomach wall (such as the glucagon like peptide 1) and stimulate the satiety center - which corresponds to our everyday experience: If the stomach is full, we feel full. Saturation signals are also sent out from the deeper intestinal sections, especially when fat is being digested. B. the hormone cholecystokinin (CCK) is involved. There are several reasons why fatty meals make you feel better: On the one hand, fat inhibits gastric emptying - the stomach stays full longer. On the other hand, strong satiety signals are sent to the brain during fat digestion.

How strongly the hunger or satiety signals work is also influenced by the fat tissue, in particular by how much fat is collected in the fat cells. The hormones ghrelin (Growth Hormone Release Inducing), amylin and leptin as well as insulin play an important role here. The signals from the adipose tissue seem to be aimed primarily at defending the fat mass: When the fat cells release fat, the appetite is strongly stimulated - so, paradoxically, bitter hunger plagues us even if we carry several hundred thousand calories of bacon reserves on our hips.

There are indications that hunger and satiety are also genetically influenced - according to the set-point theory, hunger and satiety are also based on an ideal weight that is different for each person. In addition, the Taste of food plays an important role: rats stay slim if they eat monotonous food. If they can help themselves to tasty food, they gain weight. And that also applies to people, because eating is not just an intake of food, it is also a pleasure.

The following experiment shows how important signals from the environment are when eating: If a manipulated soup plate is refilled unnoticed while eating via a hose system connected to the bottom of the plate, the participants in the experiment eat an average of 73% more soup. This tendency to finish eating makes sense in evolutionary terms - good opportunities had to be exploited to the full under the tight conditions of human prehistory. Even 5-year-old children eat according to the maxim: now or never. With big ones Portion sizes eat up to three times more!

Eating “on offer” is a big problem in today's conditions. It is estimated that humans in their evolutionary environment were adjusted to an energy density of around 107 kcal per 100 g of food - but a hamburger at McDonald’s has 287 kcal per 100 g! In concrete terms, this means: We have to learn - contrary to our evolutionary presetting - to leave a plate behind when we feel full!

Authors

Dr. med. Herbert Renz-Polster in: Gesundheit heute, edited by Dr. med. Arne Schäffler. Trias, Stuttgart, 3rd edition (2014). | last changed on at 12:55