Food addiction or fiction? Lessons from tobacco, alcohol and other drugs

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Dr. Mark Gold

In the early 1980s, it became clear to me that appetite was related to drugs of abuse. After we detoxified people with opiate addiction, those who stayed drug-free reported increased appetite and weight. During intoxication and chronic use, appetite diminished. Progressively, drug use competed with food, and users ate sporadically and for survival. We also found that cocaine use and dependence were associated with weight loss.

In the mid-1980s, I was interested in whether overeating highly palatable foods might cause an "auto-addiction." The brain might be as unprepared for very energy-dense, fatty, sugary foods as it is for cocaine. The brains of people addicted to food might release dopamine in response to cues like seeing a fast food restaurant on the highway, compelling them to stop.

The brain was the forgotten organ in overeating and obesity discussions, just as it was with tobacco, where much of the focus was on lung health, cancers and exotic treatments. Our research found that cigarette smoking caused appetite change and weight loss and smoking cessation caused weight gain, lasting for a year or longer. Researchers began to focus on smoking cessation-related weight gain because that was a big concern for many smokers who wanted to quit.

With club drugs such as Ecstasy and methamphetamine, it was more of the same and then some. These drugs not only reduced appetite; they also changed brain signaling to the point that some users had to be reminded to eat or drink. Cannabis and alcohol, which stimulate appetite, appeared to have different acute and chronic effects. With dependence, appetite and weight decreased. It was clear that all drugs of abuse caused changes in food intake, reinforcement and body mass index. Abstinence-based drug treatment was followed by overeating and weight gain. Our treatment programs started diet and exercise counselling programs for all patients.

Although the relationships among drugs of abuse and drug withdrawal, eating and body mass were well known to addiction treatment professionals, obesity experts tended to focus on diabetes, obesity-related kidney disease, breast cancer and diseases related to overeating. In the early tobacco research days, we argued that the National Cancer Institute was wasting funds that could be better spent on tobacco-related brain research, education and prevention.

As public health attention, the law and biomedical research helped us to change the course of the tobacco-smoking and related disease epidemic, we lost sight of the relationship between smoking and body mass and the number of obesity-related deaths and diseases in North America and beyond. Disease and death related to smoking decreased, whereas obesity-related disease and death increased. The pace was mind-boggling, and National Institutes of Health analysts and researchers speculated about when obesity-related deaths would outpace those related to tobacco and whether the obesity epidemic would bankrupt the health system. While tobacco-related disease usually cuts off the last seven years or so of a person's life, that person would until then have had a productive life with few health issues. But for an obese person, the diseases start early and continue throughout life. Adult-onset diabetes became so common among young people that the name was changed to type II diabetes. The "diabetes epidemic" related to overeating and obesity is now global. But what causes "globesity"?

We proposed that hedonic, great looking, smelling and tasting foods cause changes in the brain similar to what happens with alcohol or other drugs. We thought that chronic dopamine release after drug-taking would be a useful model from which to understand eating, overeating and continued compulsive eating despite dire health consequences. Why does overeating not respond to physician concerns and admonitions? This was a common complaint with tobacco: Why wouldn't patients just stop smoking and save their health and lives? In hindsight, it is easy to answer: The brain responds to smoking and the chemicals in smoke or great food with dopamine, released over time. Animals avidly self-administer drugs of abuse, as well as glucose, fructose corn syrup and fats, sometimes to the point of bingeing. Abstinence from sugar or drugs can produce withdrawal symptoms. Naloxone, used to treat opiate addiction, can provoke opiate withdrawal-like signs in opiate-using humans and, surprisingly, in opiate-naïve sugar self-administering animals. Hedonic overeating targets the brain, not the pancreas and liver, stimulates its own taking and makes continued compulsive use more likely.

Many other researchers have become interested in food and addiction. Studies of pre-bariatric patients have found a dearth of substance abusers, as though obesity were a protective factor. But bariatric surgery itself appears to be a risk factor for new cases of alcohol abuse and dependence, depression and suicide. Why bariatric surgery works remains unknown, but looking at brain changes is the logical place to start. Of considerable interest have been the diagnostic criteria for food addiction, correlation of the "diagnosis" with fMRI changes and the promise that food addicts might respond to treatments similar to those used for alcohol and other drug addiction.

We have considered obesity not as one disease, but as a number of diseases that increase body mass. We have proposed that overeating might be a food addiction that shares a common neurobiology with addiction to alcohol and other drugs. New treatments that would inhibit drug reinforcement might also inhibit overeating of some foods. Patients, once diagnosed, would be treated with addiction-like counselling, possibly surgery and anti-relapse medications. As part of their recovery program, patients might need detoxification from their current reinforcing food diet and a regimen of healthy eating and exercise.

Mark S. Gold, M.D., is chairman of the Department of Psychiatry at the University of Florida, where he is also the Donald R. Dizney Eminent Scholar in the College of Medicine and the McKnight Brain Institute.

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This page contains a single entry by editor published on March 15, 2012 8:00 AM.

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