
We often hear that junk food is addictive because of how good it tastes—the satisfying crunch of fries or the dopamine rush from a juicy burger. But according to a new study from scientists at the University of California, Berkeley, losing the pleasure of eating—not craving it—might actually contribute to overeating and weight gain over time.
Published in Nature, the study reveals a surprising discovery: long-term consumption of high-fat foods may dull the brain’s reward system, making food less enjoyable. This reduced pleasure can cause people to eat more out of habit or boredom, rather than genuine satisfaction—fueling a cycle that worsens obesity.
The researchers focused on a brain molecule called neurotensin, which helps regulate dopamine, the brain’s “feel-good” chemical linked to pleasure and motivation. In mice fed a long-term high-fat diet, neurotensin levels dropped sharply in a brain region tied to food reward.
As a result, the mice lost interest in high-fat, sugary foods—even when freely offered. This mirrors a puzzling pattern seen in some humans with obesity, whose brain scans show lower activity in pleasure-related areas when they eat.
“Our study suggests that the natural enjoyment we get from food is important—and losing that enjoyment might actually make things worse,” said senior author Dr. Stephan Lammel, a UC Berkeley neuroscience professor.
The paradox is that while high-fat diets cause weight gain, they also appear to lower food-related pleasure. In turn, this may drive people to keep eating without truly enjoying the food, creating a loop of emotional or automatic eating.
Dr. Neta Gazit Shimoni, co-first author of the study, observed this firsthand. Mice raised on fatty chow in their cages gained weight and showed a strong preference for it.
But when given a chance to eat treats like butter, chocolate, or peanut butter outside their cages—treats that normal-diet mice immediately devoured—the high-fat diet mice weren’t interested. They simply didn’t respond with the same motivation.
To explore why, the team used advanced tools like optogenetics to stimulate brain circuits that normally spark food-seeking behavior. In regular mice, this stimulation increased appetite for high-calorie foods. But in obese mice, it had no effect. That’s when the researchers discovered the missing link: neurotensin.
In healthy mice, neurotensin boosts dopamine signaling, enhancing pleasure. But in obese mice, neurotensin was nearly absent—cutting off the reward signal and dulling the motivation to eat.
Crucially, the team found ways to bring neurotensin back. When obese mice were switched to a healthier, low-fat diet for two weeks, their neurotensin levels and dopamine responses recovered.
The mice started enjoying food again and ate more mindfully. In another experiment, the team used a genetic method to boost neurotensin in the brain, which led to weight loss, reduced anxiety, improved movement, and normalized eating behavior.
“Restoring neurotensin helped regulate how and why the mice were eating,” said Lammel. “They regained the pleasure in food—but they also ate less overall, showing better balance.”
While the findings are based on mice, the researchers believe similar mechanisms could exist in humans. Past studies have shown that people with obesity often don’t get as much enjoyment from food as those at a healthy weight. This lack of pleasure may make it harder to break overeating habits.
Review and Analysis
This study offers a major shift in how we understand obesity. Instead of focusing only on cravings or lack of willpower, it highlights how brain changes—caused by diet itself—can reduce food-related pleasure and lead to disordered eating patterns.
The idea that restoring food enjoyment could help with weight loss is both fascinating and hopeful. Rather than suppressing appetite (as drugs like Ozempic do), this approach aims to bring the brain back into balance—so that people eat for joy and satisfaction, not out of habit or emotional need.
Importantly, the researchers warn against jumping to conclusions or using neurotensin directly as a drug, since it affects multiple brain areas and could have side effects. But their use of gene sequencing to find more precise targets opens the door to future treatments that could help people regain normal eating behaviors without broad or risky interventions.
This work may also be useful beyond obesity. The team is now exploring how neurotensin and dopamine circuits function in eating disorders, diabetes, and starvation—conditions where motivation and pleasure from food are deeply altered.
In a world filled with high-calorie, low-nutrient foods, this study offers a new, science-backed insight: our brains may adapt to what we eat in ways that make us eat more, not less. Helping people enjoy food again—genuinely—might be the key to changing how we approach diet and obesity treatment.
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The research findings can be found in Nature.
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