Study finds key to why obese people lose pleasure in eating rich foods

Yahoo

26-03-2025

ST. PAUL, Minn., March 26 (UPI) -- While it seems like a contradiction, many obese people do not enjoy eating rich, calorie-laden foods.
A study published Wednesday indicates that low levels of a key brain chemical among overweight patients with high-fat diets is responsible for a loss of pleasure from food.
Researchers from the University of California-Berkeley say they may have found why people with obesity have been shown to take less pleasure in eating fatty foods than those of normal weight. The culprit, they say, is a deficit of the neuropeptide neurotensin which is linked to the pleasure activator dopamine.
Neuropeptides act as a signaling molecule in the nervous system, and can affect appetite. These molecules are made up of short chains of amino acids, like other peptides, and they play a crucial role in communication between neurons and other cells.
The findings are significant because diminishing pleasure response from eating high-fat foods can lead obese patients to continue or even increase their unhealthy eating patterns "out of habit or boredom, rather than genuine enjoyment," according to the study, which was published in the journal Nature.
As counterintuitive as it may initially sound, the authors say that restoring the pleasure in eating high-fat foods via the replenishment of neurotensin actually could help reduce the progression of obesity and provide a valuable new tool in fight against the global obesity epidemic.
The need for new strategies is a stark one. More than half of adults and one-third of children and teens worldwide will be overweight or obese by 2050, according to a comprehensive study released earlier this year.
Overweight and obesity rates in adults, children and teens more than doubled over the past three decades, afflicting 2.1 billion adults and 493 million young people with excess weight.
A link between neurotensin, or NT, and eating disorders has been established in previous studies, which found that changes in NT levels are associated with obesity or eating disorders, leading doctors to believe that disrupted NT signaling may contribute to body weight disturbance.
Specifically, research has centered around the NT receptors located in a specific brain region that connect to the dopamine "reward" and "pleasure" network.
However, a key question remained: Does a high-fat diet somehow influence the release of NT in the brain? The new study, led by Stephan Lammel, an associate professor of neurobiology at UC Berkeley's Department of Neuroscience, presents evidence that the answer to this question is yes, leading to hopes that by "upregulating" NT -- perhaps through dietary changes or genetic manipulation -- the pleasure of eating can be restored.
Lammel said the study, which was supported the National Institutes of Health, the McKnight Foundation, the One Mind Foundation and others, has "uncovered a concrete mechanism that may link chronic high-fat diet exposure to a loss of pleasure in eating -- a phenomenon that's been observed for years but lacked a clear explanation."
Specifically, the researchers found that NT becomes significantly reduced in a key brain circuit in obese mice. This reduction essentially blunts the motivational value of enjoyable foods like sugar and fat.
"What's especially compelling is that restoring neurotensin levels -- either by switching back to a regular diet or through targeted genetic approaches -- can bring back that sense of reward," Lammel told UPI in a statement. "This not only increased feeding motivation in specific contexts, but also normalized weight gain, improved mobility and reduced anxiety."
Clinically, "that's really important," he added, saying it suggests that part of the challenge in obesity may not just be overeating due to pleasure, but also continuing to eat without pleasure -- out of habit or diminished reward.
"If we can find ways to restore or rebalance neurotensin signaling in the brain selectively, we may be able to help people regain healthier eating behaviors without broadly suppressing appetite or affecting other systems," he said.
The idea that making eating more pleasurable for obese patients as a way to help them manage their weight may seem paradoxical at first, Lammel admitted.
"After all, we often assume that the more we enjoy food, the more likely we are to overeat," he said. "But our study shows that the reality is more nuanced. What we found is that in mice exposed to a chronic high-fat diet, the brain's reward response -- particularly in circuits involving dopamine and neurotensin -- becomes blunted," but even so, they kept on eating the unhealthy food.
This uncoupling of reward from consumption is important "because it suggests that overeating in obesity isn't always driven by pleasure -- it can become automatic or habitual, which makes it harder to regulate."
So, the paradox is that bringing back the "right" kind of pleasure -- this is, pleasure that's appropriately tied to the reward value of food -- may actually help break the cycle of mindless or habitual overeating, the study team found.
"It's not about encouraging indulgence, but about restoring balance," Lammel said. "If food becomes pleasurable again in a meaningful and regulated way, the body may naturally recalibrate toward healthier patterns of intake."
Another prominent researcher of the connection between NT, dopamine and obesity said the UC Berkeley study represents a significant advancement in the understanding of the role brain chemistry plays in determining our eating habits.
Gina Leinninger, a professor of physiology and leader of the Leinninger Laboratory at Michigan State University's Neuroscience Program, is an expert on how neurons in the brain's hypothalamus regulate energy balance, and how disruption of these neurons contributes to the development of obesity and metabolic disease.
Leinninger, who was not connected to the study, told UPI the work sheds a new light on what had been known previously.
"Neurotensin has long been connected to modulating feeding, but how and where has remained a mystery," she said. "This work makes important strides in connecting neurotensin to the dopamine system that shape show much we want to eat, and therefore how much we do it."