Obesity starts in the brain: Here's why

Obesity starts in the brain: Here's why
Photo b Brook Lark

Two main brain systems control feeding behavior. The homeostatic system ensures the body gets the right amount of energy to maintain balance, while the hedonic system drives eating based on pleasure.

These systems are closely connected and sometimes conflict, as pleasurable foods can override feelings of fullness, leading to overeating. This complex interaction between hunger and enjoyment helps explain why people continue eating even when they are no longer hungry.

Foods high in fat and sugar, such as chocolate and ice cream, encourage overeating. This combination is rare in nature, but it is a feature of many processed foods. The availability of such calorie-dense foods has greatly contributed to the obesity problem.

Some researchers suggest that regularly eating these highly rewarding foods could cause a loss of control over food intake, leading to what might be called food addiction.

While this idea is still under investigation, it suggests that repeated exposure to high-calorie foods may override the body's natural hunger cues.

It's complicated stuff – but hang on/read on – you can do it.

The brain mechanisms behind our feeding behavior
Feeding behavior is controlled by complex brain circuits that ensure we eat when necessary and stop when we have consumed enough.

These aforementioned systems – homeostatic and hedonic circuits – are interconnected within the hypothalamus.

The hypothalamus is a small, deep-seated, and "old" part of the brain that helps keep our body in perfect balance. It acts as the body’s control center by managing things like body temperature, hunger, thirst, sleep, and emotions. It also controls when to release hormones, helping with stress, growth, and reproduction.

The homeostatic feeding system in the brain regulates energy balance by responding to signals from the body’s energy reserves; the hedonic system influences food intake based on the pleasurable aspects of eating.

Together, these systems help determine when and why we eat, balancing our nutritional needs with the enjoyment of food.

The homeostatic feeding circuit: Energy regulation and hunger signals
The homeostatic feeding system is primarily controlled by two groups of brain cells in the hypothalamus (located in the arcuate nucleus and the paraventricular nucleus).

Within these areas, two populations of neurons are crucial for regulating feeding behavior. One sort of neuron stimulates hunger when energy levels are low, promoting food intake, while another suppresses hunger when energy stores are sufficient.

Signals like low blood glucose promote feeding by activating the first kind of neurons. The neurons that suppress hunger, on the other hand, are activated by satiety signals, like increasing insulin levels, and reduce food intake when the body’s energy needs are met.

So hunger and satiety are two opposite feelings, at any time regulated by the balance between the two sorts of neurons. For example, when food is detected, the hunger neurons are inhibited, and the satiety neurons are activated to reduce the urge to eat (and thanks for that!).

This dynamic system helps ensure that feeding behavior aligns with the body's energy needs.

Recent research has shown that these neurons are far more diverse than previously thought, with distinct subtypes playing specialized roles in energy regulation, stress response, and reward processing.

The hedonic feeding circuit: Reward and pleasure in eating
In addition to hunger-driven eating, we often consume food for its pleasurable taste, regardless of nutritional need.

This is controlled by the hedonic feeding system, which involves another hypothalamus area and the dopamine system.

Dopamine, a signal molecule in the brain – also called a neurotransmitter – is the main mediator of the reward feeling and plays a central role in this system.

Neurons in the hedonic part of the hypothalamus send signals that stimulate our dopamine-releasing neurons. Dopamine drives the craving for highly palatable foods, such as sweets and fatty foods, even when the body does not require energy (like that chocolate bar you engulf, lying on the sofa at 10 p.m.).

Dopamine release in response to food cues, such as the sight or smell of desirable food, reinforces this behavior, encouraging overeating.

Our brain is a fast learner, especially when dopamine is involved. Mostly that is a good thing – but sometimes it is not. The dopamine-driven mechanism that makes us overeat can become more pronounced with repeated exposure to certain foods.
That is because the brain creates learned associations between food cues and the pleasure of eating.

Over time, this can lead to habitual overeating, as people may continue to eat despite feeling full. High-fat diets, in particular, can alter dopamine signaling, making food even more rewarding and difficult to resist.

So can the hedonic feeding system override the homeostatic feeding system?

Interaction between homeostatic and hedonic systems
Although the homeostatic and hedonic feeding systems are distinct, they do not function independently.

In fact, they interact with each other to shape our eating behaviors together. For example, hunger signals from the homeostatic system can enhance the rewarding properties of food, making eating more pleasurable – as if the food tastes better – when we are hungry.

Conversely, signals related to satiety can reduce the pleasurable effects of food, curbing overeating. So, the first chocolate bar does taste better than the third.

The interactions between these systems are complex and involve various brain regions. Ghrelin, a hormone released during hunger, not only stimulates the homeostatic hunger neurons in the hypothalamus – but also enhances dopamine release in the brain's reward centers. Thereby, hunger stimulates both the homeostatic and hedonic feeding systems.

Similarly, leptin, a hormone released when energy stores are full, can modulate dopamine signaling, reducing the drive to seek food.

It is thought that the much higher-than-natural dopamine release from our modern (high-fat/sugar) food disrupts the delicate balance between the homeostatic and hedonic systems.

And yes, then the hedonic, dopamine-driven system does override our basic homeostatic system, leading to excessive consumption of food.

Disruptions in feeding regulation: Genetics and environment
In some cases, overeating results from genetic or environmental factors that disrupt the regulation of these feeding systems.

Certain genetic conditions, such as leptin hormone deficiency, can cause individuals to feel constant hunger and eat excessively.

Leptin is the hormone that signals to the brain when the body has enough energy. But in individuals with leptin deficiency, this signal is absent, leading to uncontrolled eating. Similar trouble is seen in leptin resistance, where the body’s leptin receptors do not function properly. Both conditions are painful, not the least mentally – imagine having constant hunger...

Other factors, such as the consumption of highly palatable foods, can also lead to overeating. Foods high in sugar, fat, and salt are particularly effective at stimulating the reward system, making it difficult to resist eating even when full.

This phenomenon, often referred to as the "dessert effect," highlights how the pleasure derived from food can override feelings of fullness.

Emotional states, such as stress or boredom, can further drive this behavior, leading individuals to seek comfort in food, often in the form of sweet or fatty treats.

Addiction mechanisms in overeating
Addiction research has revealed parallels between drug addiction and overeating – brainwise.

Just like highly palatable foods, addictive drugs stimulate dopamine release in the brain’s reward centers, reinforcing whatever the desire.

Neuroimaging studies support this idea, showing that certain brain areas involved in reward processing are more active in individuals with obesity.

This suggests that overeating may, in part, be driven by a brain system that is overly sensitive to the rewarding aspects of food, much like the brain circuits involved in addiction.

Obesity treatments that treat the brain
Obesity treatments are evolving with drugs that target specific systems in the brain and body to control food intake and weight.

One of the most promising classes of drugs uses drugs that stimulate the GLP-1 receptor. Stimulating this receptor helps reduce appetite by acting on the brain’s appetite centers.

GLP-1 is naturally a hormone released by our guts, which decreases food intake and promotes a feeling of fullness. However, its natural effects are short-lived, limiting its usefulness in obesity and overeating.

By contrast, the drugs provide a longer-lasting effect on the brain regions, especially in our homeostatic feeding system. They work by reducing hunger signals and slowing digestion, helping to control blood sugar and prolong feelings of fullness.

Interestingly, chronic use of these drugs can lead to changes in brain activity, especially in the hedonic feeding system. This can lead to an increased desire for palatable food, which may encourage overeating despite reduced hunger. Sort of like – if you reduce the natural sense of hunger, you promote the desire to eat. It's pretty darn complicated.

As you see, the brain is the master of what, why, when, and how much you eat. The rest of the body is just "the puppet." That's one of the things that makes obesity such a complex condition.


About the scientific paper:

First author: Garret D. Stuber, USA
Published: Neuron, April 2025
Link to paper: https://www.sciencedirect.com/science/article/pii/S0896627325001825