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“Most of us simply fail to hold ourselves in check,” says Emmanuel Pothos. Photo: iStockphoto
Ask The Professor
Is obesity the result of an addiction to food?
Emmanuel Pothos, assistant professor of pharmacology and experimental therapeutics at the School of Medicine, tackles this month’s question:
First, why do we care so much about obesity and addiction today? It’s because a staggering 60 percent of the population in this country—and increasing numbers in other countries, both developed and developing—have become overweight or obese in the last three decades.
Until relatively recently, the research community considered obesity as a disturbance of the body’s ability to regulate body weight. Those mechanisms are known to reside in the hypothalamic nuclei in the brain. It’s clear now that the body’s normal mechanism to regulate weight is no longer the only factor at work.
Thanks to epidemiological studies, we know that obesity is not just a form of energy imbalance. At the same time, educating people about energy balance (“do not eat more than you can burn”) has failed abysmally for most of the population, despite it being a simple rule made even easier by widespread food nutrition labeling.
Most of us simply fail to hold ourselves in check. We overeat despite knowing of adverse consequences. We progress from occasional snacks to chronically eating “junk food” and less and less often practice healthy nutrition.
Compare that behavior with the criteria for drug addiction in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), which lists the three stages of addiction as preoccupation/anticipation, binge/intoxication and withdrawal/negative affect. They are characterized, respectively, by constant cravings and preoccupation with obtaining a drug; using more of the substance than necessary to experience the intoxicating effects; and experiencing tolerance, withdrawal symptoms and decreased motivation for normal life activities. A strong element of compulsive behavior is associated with drug addiction, as the individual engages in the behavior again and again despite knowing its adverse effects.
Following that definition, obesity is at least partly a form of addiction.
And there’s more. We have systemically worked on this question for the last 10 years and discovered that the brain system that mediates drug addiction—the midbrain dopamine system and its projections—is actually defective in obese and obesity-prone animals and humans very early in life.
Release of dopamine in these systems induces pleasure, which is what we pursue in life. There is simply not enough dopamine being released in these areas in the obese brain, so an individual would have to consume more and more food to try to compensate for that defect and increase dopamine release.
Compulsive eating, like a drug of abuse, can be a dopamine releaser in the brain. And that is a crucial element of dietary obesity. A possible therapeutic intervention we explore is whether one could calibrate the deficient dopamine system in an obesity-prone individual very early in life or even in utero.
