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“Because of the increasing rates of obesity, unhealthy eating habits, and physical inactivity, we may see the first generation that will have a shorter life expectancy than their parents.”

U.S. Surgeon General,
Richard Carmona,
March 2004


Bart Hoebel, Ph.D.

2009 Summit video presentation

Professor of Psychology and Neuroscience,
Princeton University.

Bart Hoebel is a Professor of Psychology, in the Program in Neuroscience, at Princeton University. His academic degrees are an AB from Harvard University, PhD from the University of Pennsylvania and an honorary doctorate from the University Catholique de Louvain, Belgium. He is a past president of three academic societies: The Neuroscience and Comparative Psychology Division of the American Psychological Association, the Society for the Study of Ingestive Behavior and the Eastern Psychological Association.

Having graduated from the University of Pennsylvania in 1962, Professor Hoebel has been at Princeton ever since. There he has conducted the research outlined below and raised a family of three with his wife Cindy. Bart is an avid skier and peace activist. He grows pine trees and built a hot air balloon and steam calliope, followed recently by rebuilding a steamboat as a floating classroom to teach clean-water ecology.


Professor Bart Hoebel will present ten years of work from his laboratory showing the first series of experiments designed to test the theory that sugar can be addictive. When rats are food deprived daily for 12 h, miss “breakfast,” and then drink 10% sucrose with their chow, they binge on the sugar every day. As a result, dopamine is repeatedly released in sugar-bingeing rats in a manner that is similar to the response to addictive drugs. After a few weeks of daily bingeing, the animals show neurochemical adaptations in the brain. Again, these changes are similar to what is seen with addictive drugs. In addition, naloxone, a drug that block’s the brain’s opioid receptors, produces signs of withdrawal with teeth chattering, anxiety and concomitant changes in dopamine release similar to morphine, alcohol or nicotine withdrawal. After two weeks of sugar abstinence, these rats will consume more sugar than before. If they cannot get sugar, they show extra hyperactivity in response to amphetamine and are prone to drink alcohol. Thus, intermittent bingeing on sugar can cause dopamine sensitization and opioid dependency, with withdrawal symptoms and long lasting aftereffects. Bingeing on sucrose does not cause obesity; the rats compensate for the added calories by eating less lab chow. But, if the sugar is high-fructose corn syrup, then the animals do gain excess weight. If the rats are bingeing each day on a sweet high-fat diet, this too causes extra weight gain, but the withdrawal signs are not evident. Thus the relation of sugar addiction to obesity is interesting, complicated and depends on the diet.

Unfortunately it has as been difficult to obtain government research funds for this controversial topic. It raises the big question of “natural addictions” in general. If sugar can be addictive, what about fat, salt, sex, and gambling? Are obese people addicted to food? Is it a “disease” like drug addiction? Will it affect insurance payments? The current empirical evidence strongly supports the concept of sugar addiction, but only in rats so far, not people. However, binge eating is apparent in the obese, bulimics and the general population. Although sugar addiction would not be as life disruptive as heroin or cocaine addiction, it may be more pervasive. It is interesting that some of the same brain adaptations seen in drug or sugar addicted animals are also seen in human addicts or obese people. This suggests that some, not necessarily all, of the underlying mechanism are the same (see our review in the Journal of Nutrition, 2008). The crucial experiments that we would like to perform to test the addiction-obesity hypothesis would investigate high-fructose corn syrup. Rats do readily consume it, and it does cause obesity, but funds are needed to determine if it has addictive properties in our binge-eating model. If the dietary and behavioral causes of sugar addiction were better understood, then better behavioral therapies could be devised using our animal model and better pharmaceutical therapies could be devised based on the underlying neuroscience. This, in turn, would help to reduce the incidence of obesity and the medical problems inherent in being overweight. Basic animal research would contribute to both preventive medicine and therapeutic pharmaceutical medicine.


The central purpose of Hoebel’s laboratory research is to reveal principles of nervous system function in the control of motivated behavior patterns such as feeding and addiction. Projects focus on the brain’s reward and aversion mechanisms, which translate physiological signals into behavior.

Self-control of brain activity

Professors Hoebel’s laboratory has studied the effects of motivated behavior on the brain; specifically the effects of eating, electrical self-stimulation of the brain and amphetamine self-injection directly into the brain. Clearly, an animal performs these behaviors to control neurochemical release and neural circuit functions in its own brain.

Measurement of neural and chemical changes during behavior

Prof. Hoebel’s laboratory pioneered in the measurement of neurochemical release in local brain sites of freely moving animals. Fluids are collected by brain microdialysis and assayed by electrochemistry. For example colleague in his laboratory have shown that dopamine is released by feeding, self-stimulation, conditioned taste stimuli that are linked to calorie input, and drugs of abuse including nicotine and alcohol.

Addiction Research

The Hoebel laboratory has discovered that drugs of abuse share a common withdrawal mechanism. In the nucleus accumbens, during withdrawal from nicotine, morphine, diazepam, alcohol and even sugar, acetylcholine levels are relatively high compared to dopamine. This is indicative of an aversive neurochemical state that the animals will work to avoid. Therefore it may be one cause of self-medication leading to drug relapse or breaking one's diet.

Sugar Addiction

Recent research has focused on the laboratory's mounting evidence for sugar dependency. Rats that binge on sugar develop signs of addiction, such as bingeing, sensitization, withdrawal and craving-like behavior. The researchers conclude that mild addiction is natural in that very sweet foods can lead to dependency under some conditions. Sugar triggers the release of dopamine and opioids. Dopamine tends to initiate food seeking, while opioids can prolong the meal. “We think that is a key to the addiction process,” Hoebel says. “The brain is getting addicted to its own opioids as it would to morphine or heroin. Drugs give a bigger effect, but it is essentially the same process.”


Drugs of abuse act on brain circuits for behavior reinforcement. Some of these circuits, such as dopamine and opioid pathways, are also used in food seeking and eating. Therefore, Professor Hoebel hypothesized that under certain conditions, such as repetitive, intermittent bingeing on very sweet food, feeding behavior might lead to a natural form of substance abuse. This animal model of food addiction may relate to binge eating disorder and bulimia in humans. His talk is designed to generate discussion of the behavioral and neurochemical conditions that can cause sugar to become a substance of abuse and its possible relation to obesity.

Sugar vs. Fat Bingeing: Notable Differences in Addictive-like Behaviors

Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake