When stress builds, reaching for “comfort food” becomes common, as we all seek something tasty to ease the tension. But have you ever wondered why that craving for high-calorie snacks seems to kick in right when things get rough?
A recent study sheds new light on this behavior, pinpointing a surprising brain pathway that may drive our impulse to eat when stressed.
In particular, the study identifies a region called the lateral habenula (LHb) as a critical part of this response.
Far from what you might expect, it turns out that this part of the brain (usually involved in self-control) might actually encourage stress eating when it’s triggered in a specific way.
The researchers focused on neuropeptide Y (NPY), a molecule in the brain that regulates appetite, and helps buffer against stress. NPY is known to have calming effects on the brain and is often released in response to anxiety. But the scientists observed something surprising: Under chronic stress, NPY started to impact LHb neurons in ways that actually fueled overeating (Keeping in mind: The typical role of the LHb is to act as a kind of “stop” signal that helps limit food intake.)
That's to say: Stress caused NPY levels to rise in the central amygdala, an area closely connected to emotional processing, and this rise in NPY altered LHb’s ability to signal satiety (or "fullness").
Essentially, the stressed LHb reduced its natural braking effect, leading to what the researchers call “hedonic feeding”—eating for pleasure rather than hunger. This change makes sense when we think of our own lives: high-stress situations often leave us craving highly palatable, calorie-dense foods that provide instant comfort.
One of the study’s most intriguing discoveries was that chronic stress didn’t just increase NPY; it also made the mice actively favor sweetened drinks over water. When given a choice, stressed mice showed a clear preference for sucralose, a calorie-free sweetener, suggesting that stress alone heightened their desire for sweets. Researchers believe this could reflect the brain’s drive to counteract negative feelings by seeking pleasure, even if the “treat” doesn’t provide actual calories. This behavior might also provide clues about how emotional eating happens in humans, especially in stressful situations when we’re more inclined to consume high-sugar, high-fat snacks.
To test how much the NPY pathway mattered, the scientists went one step further: By blocking NPY in the LHb, they found they could stop the stress-induced overeating entirely. Mice that had this pathway blocked did not show the same preference for sweetened solutions or high-fat foods.
This result highlights the NPY-LHb pathway as a potential therapeutic target. If we could safely reduce NPY’s effect on the LHb, it might be possible to prevent stress-related overeating and help with weight management, especially for those prone to stress eating.
This study offers exciting potential for treating stress-eating behaviors. By more thoroughly understanding the neurocircuitry underlying our propensity to reach for comfort foods, future treatments may be able to interrupt this pathway—allowing us to enjoy treats when we choose to, but not as a reaction to stress.
Thank you for reading,
Tim Smith MS, RD, LDN
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Citation: Ip, C. K., Rezitis, J., Qi, Y., et al. "Critical Role of Lateral Habenula Circuits in the Control of Stress-Induced Palatable Food Consumption." Neuron, vol. 111, no. 16, 2023, pp. 2583–2600. Elsevier, doi:10.1016/j.neuron.2023.05.010.
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