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Home Exclusive Neuroimaging

A popular theory about ultra-processed foods and dopamine just took a major hit

by Vladimir Hedrih
November 2, 2025
in Neuroimaging
[Adobe Stock]

[Adobe Stock]

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A neuroimaging study of young, healthy adults showed that consuming a milkshake did not, on average, result in a significant release of dopamine in the striatum region of the brain. While dopamine levels did increase in some individuals, this variability was not associated with whether a person had a normal weight, was overweight, or had obesity. The research was published in Cell Metabolism.

Ultra-processed foods are industrially manufactured products made mostly from refined ingredients and additives, with little or no whole foods. They are often engineered to be highly palatable, so that consuming them engages the brain’s reward circuits more intensely than natural foods do.

This is usually achieved by ensuring that ultra-processed foods contain large quantities of easily digestible sugars and fats. Because humans have separate neural pathways connecting the gut to the brain’s reward areas that are triggered by fats and sugars, eating foods rich in both is often more rewarding than eating foods rich in fats or in sugars alone. This is particularly true if these sugars and fats are easier to digest than those found in natural foods, as is the case with many industrially added sugars and fats.

This intense reward potential has led to a popular theory that ultra-processed foods may be addictive. The core of this theory is the idea that their consumption elicits an outsized dopamine response in the brain’s reward regions, a surge similar in nature to that caused by drugs of abuse.

According to this model, this powerful initial reward reinforces consumption. Over time, repeated exposure is thought to cause the brain to adapt, leading to a down-regulation of dopamine receptors and a blunted response. This state, known as tolerance, could then compel an individual to consume even more of the food to achieve the same initial level of pleasure, creating a cycle of compulsive eating.

It was this hypothesis that study author Valerie L. Darcey and her colleagues set out to test. They investigated whether humans exhibited an exaggerated dopamine release after drinking a milkshake, a food frequently used in studies as a proxy for an ultra-processed product because it is rich in both easily digestible fat and sugars and often contains flavor-enhancing additives. Dopamine is a key neurotransmitter in this process; it is a chemical messenger that helps signal reward and motivation in the brain, reinforcing behaviors that lead to pleasurable or satisfying experiences.

Study participants were 50 young, healthy adults, 38 of whom were women. They were recruited to cover a full range of body mass index values, with roughly even numbers of participants with normal weight, overweight, and obesity.

After joining the study, participants were supplied with meals designed to provide the exact number of calories needed to maintain their current body weight for a period of 3-5 days. All meals were prepared in the NIH Clinical Center Nutrition Department Metabolic Kitchen with all foods and beverages weighed on a gram scale. Participants were instructed to consume all the foods and beverages they were given. Any food and beverages not consumed were returned and weighed. This procedure aimed to stabilize their diets.

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After this period, participants were admitted to the center that carried out the study for several days, where they continued taking similar meals under observation. On the day of the experiment, participants first completed positron emission tomography (PET) scans of their brains in the morning, after having fasted overnight. After that, they rested for 75 minutes, at the end of which they received a glass of vanilla milkshake to consume.

Thirty minutes after drinking the milkshake, participants had their second PET scan. They also provided ratings of how pleasant the milkshake was, whether they wanted more, and how it compared to their expectations. Participants also completed several assessments of food-related behaviors, experiences, and depression.

Results showed no significant average increase in dopamine after drinking a milkshake in the striatum region of the brain. The study’s authors focused on the striatum because it is a brain region central to the reward system that processes dopamine signals. They found pronounced differences between individuals in how their striatum reacted to the milkshake, but these differences were not associated with participants’ adiposity.

In other words, while the brains of some individuals reacted to the milkshake by releasing dopamine, the brains of others did not, and the presence or intensity of this reaction was not related to a participant’s body weight.

Data indicated that dopamine responses might be related to how hungry participants felt and how enjoyable they found the milkshake to be. The dopamine response was also found to be weakly associated with the ad libitum (free) intake of ultra-processed cookies. This means that individuals whose brains reacted to the milkshake with a greater dopamine release tended to eat more cookies later when given the opportunity to eat as much as they wanted.

Discussing the findings in the context of whether ultra-processed foods can be considered addictive, the study’s authors concluded that “post-ingestive striatal dopamine responses to an ultra-processed milkshake were likely substantially smaller than for many addictive drugs and below the limits of detection using standard PET methods.”

The study contributes to the scientific understanding of neural processes related to food intake. However, the authors note that the study did not include a control group. The design compared dopamine levels before and after drinking the milkshake. Therefore, the possibility remains that other factors could have influenced the changes in dopamine observed in some individuals.

The paper, “Brain dopamine responses to ultra-processed milkshakes are highly variable and not significantly related to adiposity in humans,” was authored by Valerie L. Darcey, Juen Guo, Meible Chi, Stephanie T. Chung, Amber B. Courville, Isabelle Gallagher, Peter Herscovitch, Paule V. Joseph, Rebecca Howard, Melissa La Noire, Lauren Milley, Alex Schick, Michael Stagliano, Sara Turner, Nicholas Urbanski, Shanna Yang, Nan Zhai, Megan S. Zhou, and Kevin D. Hall.

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