Could foods children eat change their brains? Can repeated exposure to sugar and ultra-processed foods alter children’s developing reward circuits in ways resembling the effects of addictive drugs?

An October 2026 study in JAMA Network Open provides an opportunity to revisit pioneering experiments by Bart Hoebel, Nicole Avena, and colleagues.

First, the new study. Kathleen A. Page and other investigators at Keck USC studied 46 healthy-weight children, averaging 8.7 years old. She measured ultra-processed food consumption, examined brain responses to food cues using functional MRI, and followed changes in weight and body fat over one year. According to the CDC, ultra-processed foods (UPFs) are low in dietary fiber, energy-dense, and contain little or no whole foods. They also include high amounts of sweeteners, salt, and unhealthy fats.

Children consuming more ultra-processed foods showed greater activation of the dorsal striatum, a brain region involved in reinforcement learning, motivation, and habitual behavior. Greater activation was associated with subsequent increases in body mass index and adiposity. Proof of food addiction? Not yet.

Increased activation does not always mean pathological reward processing. But could repeated exposure to highly rewarding foods alter how developing brains learn what to seek and consume?

Groundbreaking Princeton Sugar Experiments

More than three decades ago, Bart Hoebel, Nicole Avena, and colleagues at Princeton investigated whether sugar could produce addiction-like responses in laboratory rats. The rats really liked sugar. No surprise. So do most people.

But repeated cycles of sugar access, bingeing, and deprivation produced something more interesting: escalating consumption, withdrawal-like responses, and neurochemical adaptations.

Sugar bingeing repeatedly stimulated dopamine release in the nucleus accumbens. Endogenous opioid systems were also involved. In one remarkable experiment, naloxone (Narcan) precipitated withdrawal-like signs in sugar-binging rats. Sugar isn’t an opioid. Yet opioid-related mechanisms help make sugar so appealing.

The Princeton experiments established that particular patterns of sugar exposure could produce addiction-like adaptations in animals. The USC study asked if children’s habitual UPF diets induce differences in developing reward circuits.

I subsequently collaborated with Hoebel and Avena, whom I mentored at the University of Florida, to investigate the overlap between drug addiction and excessive eating.

In 2011, Avena and I published “Food and Addiction—Sugars, Fats and Hedonic Overeating.” With Hoebel and Miriam Bocarsly, we also examined overlapping diagnostic concepts involving substance abuse and overeating.

Our question was simple: Why do people continue eating when no longer hungry? Maybe people really like how the food makes them feel- “hedonic eating.”

Nicole Avena: Food Is Not Cocaine

Nicole Avena, PhD, Professor of Neuroscience at the Icahn School of Medicine at Mount Sinai and author of Sugarless, continues investigating these relationships.

Dr. Avena recently talked to me about the scientific challenge in studying overeating. Said Avena, “Food engages the same reward circuitry that drugs do–that part isn’t controversial anymore. What we’re still working out is which foods, how much, and at what age repeated exposure starts to change how the brain responds.”

That distinction matters. It seems most important when discussing children and their development of eating habits and preferences.

Avena adds, “Calling a food addictive doesn’t mean it’s the same as cocaine. It means some of the same brain mechanisms (reward, craving, loss of control) can show up with food, and that’s worth taking seriously.”

Exactly. Chocolate cake is not cocaine.

But the brain does not maintain an entirely separate reward system for every rewarding substance.

Paul Kenny’s lab extended this research, demonstrating reward dysfunction, altered dopamine signaling, and compulsive-like eating in animals exposed to highly palatable diets.

Dopamine participates in motivation, learning, and reinforcement. Endogenous opioids contribute to reward and hedonic responses. Learned cues may provoke seeking long after physiological needs have been satisfied.

Drugs and Eating

My interest began in the 1970s studying cigarette smoking-induced weight loss and then cessation-related gain. Then, in the early ‘80s, I studied patients using cocaine or amphetamines who said they lost weight because they simply forgot to eat. But during abstinence, appetite returned.

Drugs changed eating and appetite. Stopping drugs changes that back again with a vengeance.

With University of Florida colleagues, I summarized these relationships in 2011. Subsequent experimental research with Orsini, Avena, and colleagues examined increased food consumption and weight gain following chronic amphetamine exposure.

Clinical observations suggested overlapping mechanisms involving dopamine, withdrawal, reinforcement, and appetite regulation.

In 2007, Kelly Brownell and I co-chaired the Yale Conference on Food and Addiction, bringing together nearly 40 experts. Nora Volkow delivered the keynote address. Brownell and I subsequently edited Food and Addiction: A Comprehensive Handbook. Ashley Gearhardt and colleagues developed the Yale Food Addiction Scale, permitting researchers to measure addiction-like eating behaviors.

At the time, comparing food and addiction was controversial. The accepted view was that food was necessary for survival. Cocaine was not.

True. But that was never the scientific question.

Kevin Hall’s randomized inpatient study demonstrated that adults consumed approximately 500 additional calories daily on an ultra-processed diet compared with a minimally processed diet.

Importantly, obesity is not synonymous with food addiction. Some obese people don’t demonstrate addictive eating. Others show addiction-like eating without obesity.

Can the Brain Remember What We Eat?

Epigenetics offers another possible connection with eating patterns. Repeated exposure to cocaine, opioids, and other addictive drugs can produce persistent epigenetic changes in gene expression within reward circuits.

Eric Nestler and colleagues showed that addictive drugs alter gene regulation in reward circuits without changing DNA sequences. Animal studies suggest highly palatable diets may produce similar adaptations. These epigenetic changes are important, suggesting that highly rewarding diets like drugs similarly influence gene regulation and neural plasticity.

But these changes are not necessarily permanent.

Children’s Diets

Could repeated exposure to particular foods create a biological memory that makes them more difficult to resist? Possibly

Ultra-processed foods account for two-thirds of the calories American children consume, according to CDC experts. These often combine refined carbohydrates, fats, flavors, and textures engineered for palatability.

The child’s developing brain learns through repeated experience, shaping learning, preferences, and habits.

Not all ultra-processed foods are equivalent. The important questions concern which foods, which children, which developmental periods, and which exposures produce persistent effects.

The October study is provocative but small. Dietary intake was estimated, neuroimaging occurred once, and confounding remains possible.

Though we are accumulating impressive MRI data, association is not causation.

What Should Happen Next?

The science has advanced beyond our original experiments. The fundamental question remains: When does hedonic or rewarding eating become compulsive eating?

We need studies examining genetic vulnerability, early stress, food insecurity, and specific combinations of sugar and fat.

The objective is not to diagnose eight-year-olds with food addiction.

The question is no longer if food engages the brain’s reward circuitry. Of course it does.

The question is whether repeated exposure to particular foods during childhood produces lasting changes in motivation, habits, and vulnerability to compulsive eating.

And whether those changes can be prevented—or reversed.

Children cannot choose the food environment we have created for them. Adults can.