Is It Possible To Be Real Hungry At All Hours?

Do you know how hunger-satiety signals are produced? There are multiple mechanisms involved and their failure can generate an intense feeling of hunger.

We need to eat to survive, but let’s not kid ourselves: we don’t eat just so we don’t die. We eat because we like it, because our gastronomy is wonderful. We eat because eating is a pleasure. And this has a huge drawback: we eat without hunger, even if we don’t realize it.

We have “atrophied” the body’s hunger signals and we have conditioned our eating behavior not to the need to ingest nutrients, but to circumstances of various kinds : from emotional disturbances to events and celebrations in which there is much more food than people and a large number of processed foods to make them very rich.

We eat because there is food, we eat out of boredom, we eat out of craving, we eat out of anxiety and sadness. And, of course, we eat because the body asks us to. But, what is the mechanism by which it asks for it? Have we spoiled the body and misinterpreted hunger signals? And, what is much more disturbing, is it possible to be hungry, real hungry, continuously? Let’s see it.

What is hunger? How is hunger produced?

Hunger is the feeling or need to eat. This is triggered by very varied stimuli, from environmental signals (the time, the presence of food, the mood, the smell of a stew …) to physiological signals, such as the signals sent to the brain when the stomach and upper part of the intestine are empty, going through the metabolic signals.

Although today, environmental signals play a very important role, we are going to focus on physiological and metabolic signals to explain what happens inside the body when we are hungry.

Physiological signs of hunger: ghrelin

After a few hours of fasting, the digestive system (mainly the stomach) begins to release a peptide hormone called ghrelin. Ghrelin not only has the power to induce intake, but it also makes you almost fantasize about food. Due to its operation, it would be expected that the levels of this hormone would decrease after ingestion.

However, this is not always the case. In Prader-Willi disease, the main symptom is obesity caused by constant eating. It seems that the cause of persistent hunger would be a high level of ghrelin that does not decrease after ingestion. The reason for this persistent elevation is still unknown. Patients who suffer from this disease do not eat because they do, it is that they are constantly hungry. But not hunger for pecking, but hunger for “I would eat a horse with a saddle and all.”

Metabolic signals of hunger: insulin and glucagon

Hypoglycemic states are powerful stimulants of intake. Faced with the drop in blood glucose, the pancreas stops producing insulin and begins to secrete glucagon. That is, glucoprivation induces food intake.

The glucostatic hypothesis suggests that ingestion is triggered by a decrease in glucose levels, detected by glucostate (a neuron that measures the level of blood glucose).

For its part, the lipostatic hypothesis suggests that what triggers eating behavior is a decrease in the level of fatty acids available to cells. This descent is detected by the hepatic receptors and the signal is sent to the brain through the axons of the vagus nerve neurons.

And after eating? Signs of satiety

The short-term satiety signals, that is, the signals that are triggered right after ingestion, come from the eyes, nose, mouth and throat (also called cephalic factors), stomach (gastric factors), the small intestine (intestinal factors) and liver (liver factors).

These are capable of sending a signal to the brain indicating that food has been ingested and that it is in the process of being absorbed. Let’s see how each process occurs, focusing on those of greatest importance:

Intestinal factors

As digestion progresses, food passes from the stomach to the small intestine, specifically the duodenum. The duodenum controls how often the stomach empties by secreting a peptide hormone called cholecystokinin (CCK).

On the other hand, a substance produced by the cells of the digestive tract that seems to act as a signal of satiety has been discovered : the PYY peptide, which is released by the small intestine after a meal, in an amount proportional to the amount of calories ingested .

Insulin

In the nutrient absorption phase, the blood glucose level begins to increase. This causes the activity of the sympathetic nervous system to decrease and the activity of the parasympathetic nervous system to increase. Given this, the pancreas stops producing glucagon and begins to secrete insulin, to transform excess glucose into glycogen.

The way insulin becomes a satiety signal is produced by insulin receptors in the brain. These would report the amount of insulin in the blood.

Adipose tissue signals: long-term satiety signals

Adipocytes, which contain a large amount of triglycerides, secrete leptin. Leptin is a hormone that has significant effects on both metabolism and food intake, acting as an “anti-obesity” hormone. The amount of leptin is proportional to body mass.

A leptin deficiency inhibits satiety signals and is an important risk factor for the development of obesity. It can be thought, then, that the treatment based on the administration of leptin will be effective for the treatment of obesity.

However, this is not the case since, in addition to having shown that the leptin levels of an obese person are not lower than those of a non-obese person, it has been shown that the problem of these patients is an insensitivity of the receptors of leptin.

Man with hands on his belly because he is very hungry

Congenital leptin deficiency: eternal real hunger

It is a very rare hereditary disease caused by a mutation in the LEP gene located on chromosome 7, which is transmitted by autosomal recessive inheritance. Children with this disorder are born with a normal weight, but they soon begin to show symptoms. Among them, the following:

Hyperphagia
Early-onset obesity.
Hyperinsulinism.
Hypothyroidism
Hypogonadism
Diabetes.

In this case, the treatment of choice is the administration of leptin or leptin analogues, since these patients do not have problems with leptin receptors but simply lack this hormone.

It’s not you, it’s your… chaotic signals?

I know this is a somewhat bold statement, but I also know that it is reassuring to know that the extra pounds are not your fault (at all). The way we feed ourselves is far from being a natural way for the body, so it is possible that all these natural mechanisms have gone a bit crazy.

We live in an era in which we feed ourselves almost out of duty, instead of listening to what the body asks for. In which the frenetic pace at which we live marks and alters almost all biological processes. For this reason, we must pay special attention to the body, to what it tells us and asks of us and the way we give it to it.

It is better to postpone mealtime to a time when we can eat consciously (to facilitate the appearance and interpretation of all these signals that we have talked about), than to eat without hunger and quickly (without giving time for them to occur. signs and being aware of them) so you can keep running through life.