Why do we eat when we are not hungry? The Neuroscience of Hedonic Eating

By Marta Solana

We often think of eating as a very simple process. When we are hungry, we eat and we stop eating when we are full. However, why do we find ourselves constantly snacking while watching TV? Why, despite feeling full, do we always have room for dessert? And why does the sight or smell of food suddenly make us hungry, even when we weren’t thinking about eating before?

These questions have become increasingly relevant in today’s world. where highly processed foods are easily available, portions are larger, and food cues are everywhere. As a result, many of us eat not to satisfy hunger, but in response to powerful cues and internal drives we may not even be aware of¹. Behaviors like this can contribute to metabolic disorders like obesity². To understand the root of the problem, we need to look beyond our stomachs and into our brains. This article explores the two systems that regulate our eating: one that keeps us alive, and one that makes food enjoyable, and sometimes irresistible.

Balancing Biology

At the core of our eating behavior are two systems of food intake regulation: homeostatic and hedonic eating. Homeostatic eating is involved in energy balance and survival, while hedonic eating is driven by the brain’s reward system, independent of energy demand. These two pathways are intertwined, allowing hedonic properties such as smell, taste, and texture to override homeostatic hunger cues³. Understanding how these systems influence our eating habits can help us navigate a world where our biology is wired for survival, but our environment is designed for indulgence.

The Homeostatic Regulation of Hunger

Hunger isn’t just the feeling of a growling stomach; it’s a complex and regulated biological response. The hypothalamus is the master regulator of homeostatic hunger (Fig. 1). Its arcuate nucleus (ARC) acts as a control center involved in processing peripheral signals to determine whether we need to eat or not. This nucleus contains two major populations of neurons. The first population consists of Agouti-related peptide and Neuropeptide Y (AgRP/NPY) co-expressing neurons. These are orexigenic, or hunger-inducing, neurons. They sense ghrelin, a hormone secreted by the stomach that signals hunger, get activated, and promote feeding behavior. The second population consists of Pro-opiomelanocortin (POMC) neurons, which are anorexigenic, or satiety-inducing, and get activated by insulin, a hormone released after eating that suppresses appetite⁴˒⁵.

Overall, this hypothalamic pathway maintains the balance between food intake and energy expenditure. However, hunger is not as black and white, as hedonic mechanisms can override this system, leading to food intake despite no true hunger present.

When Cravings Win: Why Hedonic Eating Overrides Satiety

So, if the hypothalamus dictates when to eat and stop, why don’t we always listen? The answer lies in the brain’s reward system, involved in motivation and reward. At the core of this system is dopamine, a neurotransmitter involved in motivation, learning, and reward. When we eat something delicious, dopamine is released in a region called the nucleus accumbens (NAc), reinforcing that behavior and encouraging repetition.

But there is a catch to this type of response. The more we stimulate this pathway, the more it adapts. Over time, dopamine receptors in the NAc desensitize or internalize, meaning that it takes more food to achieve the same level of satisfaction (Fig. 2). This is the same reward circuit involved in reinforcing behaviors like sex, social bonding, and drug addiction⁶. This raises an important question: can food be addictive? While food isn’t addictive in the same way as substances like nicotine or cocaine, highly processed foods rich in sugar and fat seem to activate the same neural mechanisms of habit formation and compulsion⁷˒⁸. In a world filled with tempting cues, our reward circuits can easily override fullness, not because we’re weak, but because our brains are doing exactly what they evolved to do.

Eating Our Feelings: Triggers Beyond Taste

Hedonic eating isn’t just about pleasure and taste; emotions, environment, and even the people around us can push us towards food, whether we’re hungry or not. Everyone has probably experienced how boredom or stress suddenly makes you hungry. Stress, in particular, elevates levels of cortisol, the body’s main stress hormone, which can enhance dopamine release in the brain’s reward system, making comfort eating a neurochemically reinforced behavior⁹˒¹⁰˒¹¹. The amygdala, our emotional control center, also interacts with these reward pathways, reinforcing stress-driven eating. So, when stress levels spike, your brain seeks comfort, and for many, that comfort comes in the form of chocolate or a lot of ice cream. But it’s not just emotions pulling the string, as social settings can shape what and how much we eat, too. Have you ever noticed that you eat more when dining with friends than when eating alone? Social interaction itself can activate dopamine pathways, especially in positive social contexts, subtly reinforcing shared eating behaviors. Research shows that sharing a meal with another person can increase portion sizes by 44%¹²˒¹³. Social norms, distractions, and the desire to match others’ eating habits all play a role. All in all, whether it’s stress, social influence, or boredom, our eating behaviors are thus shaped by far more than just hunger.

Understanding Our Eating Habits

Our eating behavior is more complicated than it seems; it’s a delicate balance between physiological needs and psychological desires. And in today’s world, where tempting foods are everywhere and reward cues are constant, understanding these influences is more important than ever.

Science is making important advancements in helping regain control of eating habits. One of the most talked-about tools today is Ozempic. This weight-loss drug mimics the effect of the hormone glucagon-like-peptide-1 (GLP-1), which triggers the release of insulin from the pancreas, regulating blood sugar and promoting satiety after eating. But what is truly interesting is that Ozempic can also act on POMC and NPY/AgRP neurons in the brain and enhance satiety signals while simultaneously modulating reward pathways, reducing hedonic influence¹⁴. People taking such drugs not only report eating less but also think about food less frequently, suggesting that ozempic-like drugs can blunt the reward food pathway¹⁵˒¹⁶. But while medications like Ozempic can be helpful, they are not a cure. They come with potential side effects, are not suitable for everyone, and don’t necessarily address the emotional roots of hedonic eating. That’s why generating awareness remains one of our most powerful tools.

Recognizing that overeating is not simply a lack of willpower, but the result of evolutionary wired systems interacting with modern-day excess, can help us approach our habits with awareness and empowerment. Because in the end, eating isn’t just about fuelling the body, it’s about understanding the mind. And the more we learn about the brain, the better equipped we are to find balance between need and desire.

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Further reading

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2. Morales, I. (2022). Brain regulation of hunger and motivation: The case for integrating homeostatic and hedonic concepts and its implications for obesity and addiction. Appetite, 177, 106146. https://doi.org/10.1016/j.appet.2022.106146 ↩︎
3. Campos, A., Port, J. D., & Acosta, A. (2022). Integrative Hedonic and Homeostatic Food Intake Regulation by the Central Nervous System: Insights from Neuroimaging. Brain Sciences, 12(4), 431. https://doi.org/10.3390/brainsci12040431 ↩︎
4. Konturek, P. C., Konturek, J. W., Cześnikiewicz-Guzik, M., Brzozowski, T., Sito, E., & Konturek, S. J. (2005). Neuro-hormonal control of food intake: basic mechanisms and clinical implications. Journal of Physiology and Pharmacology, 56(Suppl 6), 5–25 ↩︎
5. de Solis, A. J., Del Río-Martín, A., Radermacher, J., et al. (2024). Reciprocal activity of AgRP and POMC neurons governs coordinated control of feeding and metabolism. Nature Metabolism, 6, 473–493. https://doi.org/10.1038/s42255-024-00987-z ↩︎
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8. Stice, E., Spoor, S., Bohon, C., Veldhuizen, M. G., & Small, D. M. (2008). Relation of Reward From Food Intake and Anticipated Food Intake to Obesity: A Functional Magnetic Resonance Imaging Study. Journal of Abnormal Psychology, 117(4), 924–935. https://doi.org/10.1037/a0013600 ↩︎
9. Dallman, M. F., Pecoraro, N., Akana, S. F., la Fleur, S. E., Gomez, F., et al. (2003). Chronic stress and obesity: A new view of “comfort food.” PNAS, 100(20), 11696–11701. https://doi.org/10.1073/pnas.1934666100 ↩︎
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14. Dong, Y., Carty, J., Goldstein, N., et al. (2021). Time and metabolic state-dependent effects of GLP-1R agonists on NPY/AgRP and POMC neuronal activity in vivo. Molecular Metabolism, 54, 101352. https://doi.org/10.1016/j.molmet.2021.101352 ↩︎
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