How Junk Food Changes Your Brain- And How to Reverse It

Overeating and the rise in obesity rates in our society are frequently attributed to the dopamine rush that comes from eating junk food, such as a delicious burger and salty, greasy French fries. According to a recent study conducted by researchers at the University of California, Berkeley, eating for enjoyment- even junk food- is essential to keeping a healthy weight in a culture that is overflowing with inexpensive, high-fat foods (1^✔ ✔Trusted Source
Changes in neurotensin signalling drive hedonic devaluation in obesity

Go to source). Ironically, anecdotal data indicates that individuals who are obese could like eating less than those who are normal weight. When given food, obese people's brain scans reveal less activity in areas of the brain linked to pleasure; this pattern is also shown in research on animals.

A decrease in neurotensin, a brain peptide that interacts with the dopamine network, may be the root cause of this phenomena, according to UC Berkeley researchers. They have also discovered a potential method to bring back the enjoyment of eating while lowering total consumption.

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Having a High-Fat Diet for a Prolonged Period Takes Away the Pleasure of Eating

According to the study, a long-term high-fat diet can decrease the desire for high-fat, sugary foods, even when they are still readily available, by exposing an unexpected brain mechanism. The researchers hypothesize that the loss of eating pleasure brought on by prolonged ingestion of high-calorie foods is the source of fat people's lack of desire. In fact, losing this enjoyment could accelerate the development of fat.

Stephan Lammel, a professor in the Department of Neuroscience at UC Berkeley and a member of the Helen Wills Neuroscience Institute, stated that while having a natural preference for junk food is not always harmful, removing it could make obesity worse.

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Lowering Brain Peptide Neurotensin Aids in Weight Loss

The researchers discovered that a decrease in neurotensin in a particular area of the brain that links to the dopamine network is what causes this impact. Crucially, they show that lowering neurotensin levels can restore the enjoyment of eating and aid in weight loss, either via dietary modifications or genetic engineering that increases neurotensin synthesis.

"A high-fat diet changes the brain, leading to lower neurotensin levels, which in turn alters how we eat and respond to these foods," Lammel stated. "We found a way to restore the desire for high-calorie foods, which may actually help with weight management."

Novel Approach for Obesity Treatment

Although results from mice don't always apply to people, this study may pave the way for novel approaches to obesity treatment by reestablishing the enjoyment of food and disrupting bad eating habits.

Neta Gazit Shimoni, a postdoctoral scholar at UC Berkeley, stated, "Imagine eating an amazing dessert at a great restaurant in Paris- you experience a burst of dopamine and happiness." We discovered that mice fed a regular diet experience the same emotion, but mice on a high-fat diet do not. Instead of eating because they truly like it, they can continue to do so out of habit or boredom.

The study, which will be published in the journal Nature, has Lammel as the senior author and Gazit Shimoni and Amanda Tose, a former doctoral student at UC Berkeley, as co-first authors.

Resolving a Long-Standing Conundrum in the Study of Obesity

Due to the failure of numerous fad diets and eating plans to yield lasting outcomes, physicians and researchers have been grappling with the understanding and treatment of obesity for decades. Among numerous unsuccessful strategies, the recent success of GLP-1 agonists like Ozempic, which reduces appetite by enhancing sensations of fullness, stands out.

Lammel focuses on brain circuits, especially the dopamine network, which is essential for motivation and reward. Because dopamine is frequently linked to pleasure, it encourages us to pursue fulfilling activities, such eating meals high in calories.

Gazit Shimoni observed a startling paradox while rearing mice on a high-fat diet: The mice gained extra weight because they preferred the 60% fat high-fat chow over regular chow, which only contained 4% fat, in their home cages. However, compared to mice on a regular diet, who promptly devoured everything provided, they displayed significantly less willingness to indulge when removed from their home cages and allowed unrestricted access to high-calorie goodies like butter, peanut butter, jelly, or chocolate.

"If you give a normal, regular-diet mouse the chance, they will immediately eat these foods," Gazit Shimoni stated. "We only see this paradoxical attenuation of feeding motivation happening in mice on a high-fat diet."

She learned that although this impact had been documented in earlier research, no one had investigated its cause or relationship to the obesity phenotype seen in these animals.

Restoring Neurotensin Restores the Brain Alterations Brought on by Obesity

Lammel and his colleagues employed optogenetics, a method that enables researchers to manipulate brain circuits using light, to study this phenomenon. They discovered that while stimulating a brain circuit that links to the dopamine network made mice on a normal diet want to consume more high-calorie items, obese animals showed no change in response to the same stimulation, indicating that something must have changed.

They found that the reason was that in fat mice, neurotensin was so low that dopamine was unable to provide the typical pleasure response to diets high in calories.

According to Lammel, "Neurotensin is this missing link," Typically, it increases dopamine levels to promote motivation and rewards. However, neurotensin is downregulated in mice fed a high-fat diet, and they no longer have a strong urge to eat foods high in calories, even when they are readily available.

After that, the researchers experimented with methods to raise neurotensin levels. Obese mice's neurotensin levels, dopamine function, and desire for high-calorie meals all reverted to normal after two weeks of returning to a regular diet.

The mice dropped weight, displayed less fear, and had better mobility after neurotensin levels were artificially raised by genetic means. Additionally, their feeding habits became more typical, as they became more motivated to eat high-calorie meals while simultaneously consuming less food overall in their home cages.

"Bringing back neurotensin seems to be very, very critical for preventing the loss of desire to consume high-calorie foods," Lammel stated. "It doesn't make you immune to getting obese again, but it would help to control eating behavior, to bring it back to normal."

More Accurate Obesity Treatments

Neurotensin operates on multiple brain regions, increasing the possibility of undesirable side effects, even if it may theoretically restore food drive in obese people when administered directly. To get around this, the researchers employed a technique called gene sequencing, which enabled them to pinpoint particular genes and biochemical pathways that control the action of neurotensin in obese mice.

This finding opens the door for more targeted medications that could specifically improve neurotensin function without having widespread systemic effects, and it also presents important biological targets for future obesity treatments.

"We now have the full genetic profile of these neurons and how they change with high-fat diets," Lammel stated. "The next step is to explore pathways upstream and downstream of neurotensin to find precise therapeutic targets."

Lammel and Gazit Shimoni intend to broaden their study to look into the impact of neurotensin in conditions other than obesity, such as diabetes and eating disorders. "The bigger question is whether these systems interact across different conditions," said Gazit Shimoni. What is the impact of fasting on dopamine circuits? In eating disorders, what happens? These are the inquiries we will be examining next.

Reference:

1. Changes in neurotensin signalling drive hedonic devaluation in obesity - (https://www.nature.com/articles/s41586-025-08748-y)

Source-Medindia