O

ur eating behavior is based on biological mechanisms resulting from adaptation to an environment that has been relatively stable for many millennia.

Like all behavior, the brain is the operator. But in recent decades, these mechanisms have had to cope with changes in lifestyles that have disrupted this adaptation in the sense of an energy imbalance: intake is higher than expenditure.

This leads to energy storage in the form of fat and what some even call an obesity epidemic.

We must therefore consciously control our diet and set up a cognitive filter to avoid this energy imbalance.

And while nutrition is necessary, analyzing how we function and where our eating habits come from can help us avoid a perpetual struggle with our bodies, which are sometimes destructive, especially for self-esteem.

THE DIFFERENT STAGES OF OUR EATING BEHAVIOUR

Our eating behavior corresponds to a physiological sequence called prandial, which is controlled by the brain, especially the hypothalamus. It is a very precise sequence:

1. First, a hunger signal from the neurons in the hypothalamus brain region tells us that we need to eat. The prandial phase begins.

2.When we eat, sensory mechanisms gradually develop and lead to satiation, which interrupts the meal.

3.Then begins the postprandial phase, during which we are in a state of satiety: we have no desire to eat (for a variable period of time depending on individuals and cultures). This continues until the next signal of hunger, unless food that is too attractive is easily accessible.

preprandial, prandial, and postprandial stages

Satiation and satiety are part of the body’s appetite control system and are involved in limiting energy intake.Satiation is the process that causes one to stop eating; satiety is the feeling of fullness that persists after eating.

Any other consumption, for example, when we eat without hunger simply because of the appeal of a meal in front of us, out of boredom, or even to console us, can be considered as responding to other factors that we can call extra physiological. This implements different mechanisms related to pleasure and distraction.

THE HUNGER SIGNAL: A LACK OF SUGAR

But first, let’s look at physiology. The mechanism behind the hunger signal is still the subject of much controversy.

One of the most robust hypotheses is that of central glucopenia: a moderate but sudden drop in glucose supply to neurons in the hypothalamus (Glucose is the form of sugar that provides energy to all cells).

The hypothalamus is the brain’s “control tower” of eating behavior. It then triggers the hunger signal, communicating with many other brain regions.

In the bloodstream, a subtle but measurable decrease in blood sugar (blood glucose concentration) can be detected before a meal.

Thanks to this, in the early 2000s scientists showed that this phenomenon makes it possible to distinguish a meal from a snack: only the first is preceded by a drop in blood sugar levels.

With miniaturization, glucose measuring devices can be used in patient dietary education. This will probably benefit all those who have difficulty detecting the hunger signal that social constraints so often make them ignore or neglect.

SATIATION: THE SIGNAL THAT MAKES YOU STOP EATING

How does satiation make you stop eating?

As we’ve shown above, Satiation is the cessation of the motivation to eat. It is mainly sensory. As food is ingested, the oral cavity sends sensory stimuli to the hypothalamus neurons, which gradually dissipate until consumption is stopped.

It is therefore a phenomenon of habituation, a kind of sensory exhaustion: we are no longer motivated to eat – this food at least.

However, this motivation quickly reappears if food with new sensory characteristics (a different texture or flavor for example) is presented to us.

This explains the existence of the French-style meal, a succession of dishes, each one starting with as much appetite, even the dessert. We speak of specific sensory satiation, highlighted in 1981 by Barbara Rolls, then at Oxford University.

However, studies on animals have shown that an intestinal intermediary is necessary to stop the meal altogether. It is mainly the intestinal hormones and the vagus nerve (which connects the intestines to the brain), as well as the stretching of the stomach, that participate in Satiation.

How keeping track of your food portions promotes healthy eating habits?

First of all, what is essential to understand is that satiation is subject to learning, i.e., conditioning.

Without even paying attention, we adjust the amounts of food we consume according to the effects that our body has associated with the sensory characteristics of that food.

For example, imagine that your breakfast meal is reduced in calories without your knowledge, so that you are hungry earlier in the afternoon. If this happens again, you will unconsciously increase the amount you serve yourself for lunch.

On the other hand, for example, if you got full and couldn’t finish the food you brought to work, next time you will probably prepare less food.

In the 1980s, Jeanine Louis-Sylvestre’s team showed that this behavior is learned after only four to five occurrences. This is how we learn our sensory scales so that our food portions make sense to us.

This mechanism of satiation by learning is essential, because it protects us from over-consumption. We must allow this conditioning to take place, while maintaining a specific routine in the type of meals we have.

In fact, for animals, continually changing varieties of meals is the most effective experimental procedure to make them obese.

In 2014, Amy Reichelt of the University of South Wales, Australia, and her colleagues showed that so-called cafeteria rats, which are offered cookies, cakes,  and other sweets at will, gain more than twice as much weight as control rats. Also, their specific sensory satiation is significantly reduced.

More worryingly, even if the food is low in calories (and very high in quantity), we would be more likely to miss the protective benefit of Satiation, which would lead to consuming more calories and therefore to gain weight.

SATIETY: THE FEELING OF FULLNESS

Can satiety always prevent overeating?

The third phase of the prandial sequence is Satiety, a state of non-hunger that persists for several hours after the end of a meal. Satiety is actually the lack of dietary motivation; we don’t feel like eating. 

More specifically, consider the cost/benefit model of food behavior specialist George Collier: the onset of food motivation depends on the effort required to achieve this satisfaction.

Below a certain threshold, for example when we are in the presence of delicious, readily available food, the hunger signal is not required.

Satiety is therefore not useful in similar cases to prevent you from over-eating. The solution? Avoid having foods readily available that are too delicious and likely to restore the motivation to eat.

Why exactly we feel full? (How satiety works)

Why are we in a state of Satiety after a big meal? We already explained how the glucose concentration in the hypothalamus neurons is a factor. But other factors also allow the brain to know the energy status, i.e., when the different tissues and organs of the body have enough energy.

Those factors are signals in the form of hormones from the digestive tract, adipose (or fatty) tissue, and the pancreas:

1. Thus, the stomach releases ghrelin, a hormone that was once considered a trigger for a meal, but it is more like a “food concern” resulting from conditioning. Ghrelin concentration increases when you wait for a meal. A higher blood level of ghrelin contributes well to increasing food intake during the meal.

2. The pancreas secretes insulin, which serves as a satiety signal in the brain.

3. Finally, fat tissue produces leptin, which also contributes to the satiety signal. Discovered twenty years ago, this hormone has linked fat reserves and eating behavior. Since then, it has been shown that fatty tissue is not just an inert mass, contrary to what we thought, but an endocrine tissue, i.e., one that secretes hormones capable of communicating with our brain.

Therefore, the three factors considered to date to be crucial for the control of dietary behavior are ghrelin, insulin, and leptin. And all three act on the lower part of the hypothalamus: the arched nucleus.

It should be noted that these factors often follow a double path:

– Endocrine (in the blood between the digestive tract and the brain).

– Neuronal. i.e., through the vagus nerve, which connects the organs of the intestines to the brain. Thus, as the meal progresses and in the hours that follow, the stretching of the stomach and the stimulation of intestinal receptors send a satiating signal through the vagus nerve, which will be interpreted in the arched nucleus. 

A microchip in the stomach to lose weight

All this inspired some people, such as the creators of a chip placed in a capsule that the patient swallowed. In the stomach, this chip can be activated through a smartphone application, so that it stimulates the vagus nerve during a meal to increase the feeling of fullness and reduce the amount of food consumed.

It is not sure that this device is the appropriate response to a problem as complex as obesity, but it is likely to attract the interest of those who fail to follow dietary recommendations. 

HOW MUCH DOES THE PLEASURE FROM EATING AFFECT OUR DIETARY BEHAVIOUR

Are you eating just for pleasure, or does the need for energy motivate you to eat?

For a long time, two schools of scientists have been opposing each other on the role of pleasure in eating.

For some, pleasure is the essential motor for initiating behavior: without it, there is no motivation. For others, pleasure reinforces motivation, but is by no means necessary to trigger it: we can eat a meal that does not bring any pleasure.

Recent research seems to support the latter: pleasure is not necessary for eating behavior. 

How strong is the link between pleasure and the motivation to eat?

In the late 1990s, biopsychologist and neurobiologist Kent Berridge of the University of Michigan introduced the concept of wanting versus liking to understand the role of pleasure in food intake. 

The goal of this model is to distinguish between pleasure (liking) and motivation (wanting). Therefore, pleasure would not be a mandatory link to motivation. Pleasure and motivation would be distinct.

Moreover, the neural networks involved in pleasure and motivation are different. As proof: pleasure and motivation take place mainly in a part of the brain called the nucleus accumbens. But each in separate areas of this nucleus!

How dopamine affects our eating habits?

Dopamine is a neurotransmitter that has long been thought to be responsible for both pleasure and motivation. Dopamine does stimulate the nucleus accumbens, but only its periphery. This area is active when we want to eat.

However, it is another area at the center of the nucleus accumbens, called the hedonic hotspot (the pleasure center), which is less than one cubic millimeter in rats and about one cubic centimetre in humans, that causes pleasure. It is stimulated by opioid molecules (opium derivatives such as morphine and heroin), including those that our brain naturally releases when we experience pleasure.

Berridge has shown that opioids and endocannabinoids (the cannabis analogous produced in the brain) stimulate this small area of the nucleus accumbens and cause pleasure, independently of dopamine. But even more interesting, he revealed that it is possible to block any pleasure without extinguishing the motivation generated by the action of dopamine on the periphery of the nucleus accumbens.

How does the drive to eat when you’re not hungry can be explained?

Wanting to eat without expecting pleasure from it involves a phenomenon called incentive salience
This means that the mere presence of food can produce the will to consume it. 

Dopamine is therefore not the molecule of pleasure; it does not allow us to associate the food consumed with the pleasure it gives us. Instead, it is the mediator of dietary compulsion, that is, the motivation to eat, even when we are not hungry. 

For some individuals, even though they are in a state of satiety, the hyper-responsiveness of this dopamine-activated system would explain why food would trigger a compulsion to eat similar to the one we feel when we are hungry. 

These discoveries, therefore, show that the pleasure of eating is not an end in itself.

THE EFFECTS OF SOCIAL ENVIRONMENT ON EATING HABITS

Does eating with others makes you eat less?

Not everything is about what’s on our plate, our hypothalamus, and our fat tissue. Eating is rarely a solitary act. We like to eat with family, friends, and colleagues. The role of social factors on consumption is significant. On the other hand, their consequences are variable.

John De Castro, of Sam-Houston University in Texas, has been exploring the dynamics of food consumption in the natural ecosystem of human beings since the 1970s.

In particular, he showed that eating with other guests increases the size of the meals in proportion to the number of participants. According to him, seeing others eating would encourage us to consume, and since group meals are often more festive, we would eat more.

This seems to contradict the usual recommendations that it is better to eat as a family than alone in front of the television. However, the impact of social factors on dietary behavior is very nuanced.

For example, a series of studies conducted between 2010 and 2012 in Ile-de-France by France Bellisle, research director at INRA, and her colleagues revealed that social interaction rather reduces food consumption among young women and adolescents.

Does eating in front of the TV makes you eat more?

In the studies above conducted by France Bellisle, television increases the dietary intake of overweight or obese adolescents.

It is now well established that television promotes obesity, not only through physical inactivity and snacking, but also by stimulating mealtimes. What is the reason for this? 

Why TV snacking is bad

Distraction is a primary component of the answer. In 2013, Suzanne Higgs’ team at the University of Birmingham analyzed 24 studies on food consumption and concluded that distraction increases the amount of food consumed during the meal. And even more so the amount consumed later in the day – as if satiety was reduced. 

This effect would be largely countered if we paid more attention to what we eat. Other distractions, such as music, can increase consumption during a meal.

The practical consequences are important in particular to promote the importance of paying attention to what we eat, not to exercise excessive cognitive control, but so that the unconscious mechanisms we have described in the sections above can be expressed in a reliable and complete way. 

Moreover, if you have a pet, you know that it does not appreciate that you distract it when it eats. This is a wisdom that we should have kept, even if it seems incompatible with modern consumer habits.

PHYSICAL ACTIVITY AND IMPROVING EATING BEHAVIOUR

Physical activity regulates energy intake

We cannot conclude this overview of eating behavior without mentioning the essential role of physical activity.

As early as 1967, Jean Mayer and Donald Thomas of the Harvard School of Public Health published an essential study in Science in which they showed that rats accurately compensate for the energy expenditure caused by exercise sessions (nearly five hours a day) while eating, so that their weight is maintained.

More importantly, imposed sedentary lifestyle, i.e., the lack of physical exercise, leads to over-consumption and to a significant and rapid weight gain.

Physical activity is the link between the brain and the stomach

In fact, the link between the brain and the intestines is largely through the so-called autonomous nervous system, which is maintained by… physical exercise! 

So without physical exercise, this link is not fully functional, which means that the body does not properly adapt energy intake to expenditure. This should add to the arguments for daily physical activity. 

But do we compensate for the energy we expend during an exercise session by eating even more?

In 2013, taking up all the studies published to date, Matthew Schubert of Griffith University in Australia and his colleagues concluded that, on average, we do not compensate for energy spent while exercising. This is true for either the meal we have after working out or within 24 hours. 

In other words, energy expenditure mechanisms would primarily draw on fat reserves rather than stimulate dietary motivation.

Of course, this requires having sufficient body reserves. In contrast, the “dry” athlete (i.e., with very low body fat) recovers part or all of the energy consumed during eating. 

DOES OUR EATING BEHAVIOUR DEPEND MORE ON OUR ENVIRONMENT THAN ON OUR PHYSIOLOGY?

In 2011, De Castro estimated that the environment accounted for 86% of the food intake, reducing the share of neurobiology to the lowest level. 

It is a reductive vision emphasizes the role of the environment at the expense of biology.

However, we believe that the idea that there is no physiological response to environmental factors is false. As we have said, as fat mass increases, it produces leptin, which reduces dietary motivation in the brain. Therefore, some people do not need to restrict themselves after a few days of festive meals voluntarily, their bodies are spontaneously making this adjustment.

The interdependence of neurotransmitters and their ubiquity is making it illusory to separate internal and external factors. 

Eating behavior is the very type of integrative mechanism that struggles to be described in a simplified way. 

Yet, if we taught those in need how their bodies work with food, who knows if we would not find more solutions to the overeating problems faced by a growing part of humanity.

IN SUMMARY

Our eating behavior is based on a precise physiological sequence: hunger signal, Satiation, and Satiety. 

A central structure of the brain controls our food intake, receiving information from the stomach, fat tissue, and pancreas.

Many factors disrupt this control mechanism, for example, too much food available, too much variety, and being distracted by TV.

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