Updated April 27, 2025

Beyond the Growl: The Regulation of Hunger

Nnaemeka Ukwuoma, MD

We all know the feeling. That stomach growl that says, "Hey, it’s time to eat!" But hunger isn’t just about having an empty belly. It’s way more complicated than that.

Hunger is an ancient survival instinct, designed to keep us alive when food was scarce. Over millions of years, our bodies developed a system to make sure we ate enough to survive. But today, when food is available almost everywhere and anytime, that same system can sometimes work against us, leading to overeating and health problems.

To really understand hunger, it's important to know there's a big difference between two things: true hunger (homeostatic hunger) and appetite (hedonic hunger). Hunger is the physical need for energy, while appetite is the desire to eat for pleasure, even when your body doesn’t need more food. Both involve a complex back-and-forth between your gut and your brain (the gut-brain axis). Hunger happens through three main systems, each one fascinating in its own way.

The first is called homeostatic hunger. This is the body’s basic survival mode. When your stomach is empty, it releases a hormone called ghrelin that tells your brain it’s time to eat. At the same time, a major nerve called the vagus nerve carries hunger signals from your gut to your brain. Your brain responds by boosting dopamine, which makes eating feel rewarding. Once you start eating, your body sends different hormonal and neural signals to help you stop. Your stomach stretches, your gut releases hormones like GLP-1 and PYY, and nutrients like proteins and fats help reinforce that feeling of fullness. Blood sugar and insulin levels rise after a meal, sending one last “we're satisfied” message to your brain. Altogether, this cycle keeps your energy balance. At least, that's the idea when the system is working the way it’s supposed to.

The second system is hedonic hunger, and this one’s all about eating for pleasure. Unlike homeostatic hunger, hedonic hunger isn’t about survival. It kicks in when you eat because the food looks, smells, or tastes amazing, even if you're not truly hungry. Think about the last time you had dessert even though you were already full. That’s hedonic hunger at work. Emotions have a big influence here too. Stress, sadness, boredom, even happiness, all can trigger cravings for certain foods, especially sweet or salty ones. Our brains are hardwired to prefer these flavors because they once meant that foods were safe to eat. But in today’s world, where sugary, high-fat foods are cheap and everywhere, it can easily lead to overeating. Things like culture, upbringing, advertising, and even income level all shape how strong our hedonic hunger is. 

The third hunger system is the most surprising: microbiota-driven hunger. Your gut is home to trillions of bacteria, and they aren’t just sitting there quietly. They help regulate your immune system, your metabolism, and yes, your hunger. Certain gut bacteria can affect the release of hunger hormones like ghrelin (“hunger” hormone), leptin, and insulin (“full” hormones). Some microbes produce substances that either make you hungrier or help you feel full. Others influence the gut-brain connection by making compounds like short-chain fatty acids, which can affect hunger signals in different ways depending on how and where they bind in the body. There's even evidence that certain bacteria can produce proteins that mimic human hormones, subtly nudging your body to eat more or less. While research on the microbiome’s role in hunger is still developing, it's becoming clear that the health of your gut can have a real impact on how much and how often you want to eat.

Of course, genetics also play a role. Rare genetic conditions like Prader-Willi syndrome or mutations in the leptin gene can cause intense, constant hunger and early-onset obesity, but they account for less than 7% of childhood obesity cases. For the most, it's more about how our biology interacts with modern life.

When these hunger systems get disrupted, it can cause serious problems. Anorexia nervosa is one example. Even though the body produces high levels of ghrelin to try to trigger hunger, the brain seems to ignore the signals. It is thought that this might be due to changes in brain chemistry and even gut microbiota, making the normal hunger response break down. On the other hand, obesity often results when hedonic hunger overwhelms homeostatic hunger, leading to increased rates of heart disease, diabetes, and depression. 

Understanding hunger better is already leading to new treatments. One of the most promising are GLP-1 receptor agonists. This class of  medication has been found to be helpful for people struggling with obesity and has been demonstrated to reduce the risk of diabetes, heart disease, sleep apnea, and even improve pain from osteoarthritis. 

In the big picture, learning how hunger works opens up new possibilities for personal health, public policy, and even global food systems. It’s striking to realize that while the U.S. spends more than $800 billion a year on food and health-related industries, experts estimate that ending world hunger could cost about $100 billion a year. There’s a lot to rethink, both for our bodies and our world.

At the end of the day, hunger isn’t just a simple signal from an empty stomach. It's a rich, complex system shaped by evolution, biology, emotions, and the environment we live in. And the better we understand it, the better we can work with our bodies, instead of against them.

References:

1. Bliddal, H., et al. (2024). Once-weekly semaglutide in persons with obesity and knee osteoarthritis. The New England Journal of Medicine, 391(17), 1573–1583. https://doi.org/10.1056/NEJMoa2403664

2. Fasano, A. (2025). The physiology of hunger. The New England Journal of Medicine, 392(4), 372–381. https://doi.org/10.1056/NEJMra2402679

3. Li, M., et al. (2025). Glucagon-like peptide-1 receptor agonists for the treatment of obstructive sleep apnea: A meta-analysis. Sleep, 48(4), zsae280. https://doi.org/10.1093/sleep/zsae280

4. Lincoff, A. M., et al. (2023). Semaglutide and cardiovascular outcomes in obesity without diabetes. The New England Journal of Medicine, 389(24), 2221–2232. https://doi.org/10.1056/NEJMoa2307563

5. Malhotra, A., et al. (2024). Tirzepatide for the treatment of obstructive sleep apnea and obesity. The New England Journal of Medicine, 391(13), 1193–1205. https://doi.org/10.1056/NEJMoa2404881

6. McGuire, D. K., et al. (2025). Oral semaglutide and cardiovascular outcomes in high-risk type 2 diabetes. The New England Journal of Medicine. Advance online publication. https://doi.org/10.1056/NEJMoa2501006