Addicted to Food? Increasing Evidence Suggests Compulsive Eating, like Compulsive Drug Use, Is a Brain Disorder.
Increasing Evidence Suggests Compulsive Eating, like Compulsive Drug Use, Is a Brain Disorder


by Brenda Patoine

May 20, 2009

 

BRIEFING PAPER

              

Ann Whitman
(212)223-4040
awhitman@dana.org

             

Johanna Goldberg
(212)223-4040
jgoldberg@dana.org

Could pathological overeating be considered an addictive disorder, in which food is the “drug” of choice?            

The issue, with all its scientific, social, and even legal implications, is one of many being debated as the American Psychiatry Association readies for publication (in 2012) the latest version of its psychiatric diagnostic manual, the DSM-V.

If the idea that a juicy cheeseburger or brownie sundae can, for some, trigger behaviors that mimic addiction to cocaine, heroin or alcohol seems hard to accept, consider that one of the leading proponents of treating compulsive pathological overeating as a brain disorder is no less an authority than Nora Volkow, M.D., the director of the National Institute for Drug Abuse (NIDA) and a member of the Dana Alliance for Brain Initiatives.  Volkow, whose research has helped unravel the brain circuitry underlying compulsive overeating and drug addiction, has proposed that forms of obesity that are driven by an excessive motivational drive for food and an inability to exert self-control over these behaviors be included as a mental disorder in DSM-V. 

In an editorial in the American Journal of Psychiatry1, Volkow argues that the key characteristics of obesity—compulsive consumption of food and the inability to restrain from eating despite negative consequences to one’s health and social interactions—closely parallel currently accepted DSM-IV definitions for substance abuse and drug dependence.  Consideration of the “mental component of obesity,” she writes, is critical to developing truly effective preventative and treatment strategies.

The idea is not without controversy.  Columbia University epidemiologist and Dana Alliance member Myrna Weissman, Ph.D., is among those who believe that any steps to define obesity as a mental disorder must be taken with caution for the mildly plump.  She worries about stigmatizing people who may be only slightly overweight but may perceive themselves as obese—especially women, who face tremendous societal pressures to be fashion-model thin.  “We don’t need to give women any more trouble,” Weissman says.

Food, Drugs Both Release Dopamine

Increasing evidence from animal and human imaging studies suggests that drugs and food both trigger a sense of well-being by activating the reward circuitry of the brain, a neural pathway network of brain regions that communicate with one another largely through the release of the neurotransmitter dopamine.

In an interview, Volkow said: “In people who are pathological overeaters, the normal physiological processes that regulate one’s pattern of eating behavior have gone awry and one can no longer control one’s intake of food.  It’s no surprise that we are starting to see commonalities in the areas of the brain and the neural systems that are disrupted in these people compared to individuals who are addicted to drugs.”

Substances like cocaine or alcohol act directly on the system to create an immediate rush of dopamine.  Food acts more circuitously, activating peripheral hormones that feed back to the brain while at the same time creating a memory that links that brownie to a sensation of pleasure and satisfaction.

Working with collaborators at Brookhaven National Laboratory, Volkow first reported in 2002 that exposure to food stimuli—even a picture or smell of a favorite food—increases the release of dopamine into this system in normal-weight individuals, just as drugs of abuse do in drug-addicted individuals.  In both cases, the message to the brain is “that feels good, do it again.”

As the key chemical messenger of the reward system, dopamine influences an individual’s desire for food by modulating brain circuits involved in motivation, inhibitory control, learned conditioning, and what’s called salience attribution, or how much value is placed on a particular stimulus.  Disruptions in any one of these areas can lead to compulsive eating—or compulsive drug use—in vulnerable individuals.

That’s where cognitive control comes in.  We have to consciously override the strong impulse to seek that pleasurable feeling again (i.e., eat another brownie) even when we know we shouldn’t have another.  Recent brain imaging studies in humans have tried to pinpoint the areas involved in this willful inhibition of the impulse to eat something highly desirable, with the goal of identifying targets for interventions that might somehow pump up the ability to resist yummy foods.  Of particular interest is the orbitofrontal cortex (OFC), an area involved in controlling and planning behaviors that is regulated by dopamine signaling.  In collaboration with Volkow,  Gene-Jack Wang, M.D., of Brookhaven National Laboratory used PET imaging to track neural activity as hungry volunteers were teased and tempted by images, smells, tastes, and florid discussions of their chosen favorite foods. They found a marked increase in metabolic activity in the OFC in proportion to the volunteers’ subjective perception of their hunger and desire to eat.2

In a second study with a similar design,3  the volunteers were told to consciously quell their desire for the food being presented to them. Brain scans were performed during this willful inhibition.  To their surprise, the researchers found that men were better able than women to inhibit their desire for the presented food:  they had lower scores on self-reports of hunger and desire for the food, and PET images showed decreased brain activity in the OFC.  In women, self-reported desire and hunger measures decreased to a lesser degree than men’s, and metabolic activity in the OFC remained unchanged.

In an interview, Wang said they had not expected to see a gender effect, but the finding has prompted them to dig deeper to try to understand what might be at the root of male-female differences.  His group is repeating the study, this time controlling for hormonal influences in terms of where in the menstrual cycle the women are, in an attempt to sort out the possible mechanisms.

Chronic drug use also causes long-term neurologic adaptations, including changes in neuron structure, neurotransmitter levels, and the transcription factors that regulate genes.  These changes—thought to be part of the brain’s attempt to adapt to the increased dopamine load induced by repeated drug use—may contribute to the high rate of relapse to drug use.  Some evidence now points to similar types of neuroadaptive changes in animal models of overeating behavior, research that Michael Lutter, M.D., Ph.D., a psychiatric researcher at University of Texas-Southwestern, calls “probably the best single evidence that food could be addictive.”  Such changes might help explain the notoriously high rate of diet failure or rebound weight gain, behaviors that essentially represent a “relapse” into unhealthy eating patterns.

Wired to “See Food, Eat Food”

It’s clear that there is no single reason behind the alarming rise in obesity.  Lack of physical activity, greater availability and cheapness of food, and myriad other lifestyle and social factors play roles.  Within this mix of candidate culprits, the impact of a brain evolutionarily driven to “see food, eat food” cannot be overlooked.

In terms of survival of a species, little compares in importance to eating.  So it makes sense that the brain would be optimized over eons of evolution to respond and react to food, especially the kind of high-calorie, nutrient-dense food that would tide you over until the next time you could eat.  The evolutionary theory is that highly palatable foods were not readily available when animals were evolving, so there was a survival advantage to overeating when such foods were available. “That’s a possible explanation for the existence of this [reward] pathway,” says Lutter.

Volkow puts it this way: “Our brain did not develop for us to take drugs.  It was designed to motivate you to eat food when you see it, because in the past food was a rare commodity and you survived only if you ate the food when it was available.  Drugs of abuse hijack the pathways that evolved to encourage us to eat, particularly those related to the rewarding properties of food.”

The problem is that food, in most developed societies, is no longer rare; it is abundant, cheap, diverse, flavorful, and readily available.  We are constantly bombarded by images, smells, and messages about highly palatable food, which continually challenge our cognitive capacity to control the evolutionarily driven compulsion to eat when the impulse strikes.  Given all that, Volkow says, it’s a wonder we don’t see an even bigger problem with obesity.

“Obesity has become an issue in part because we have kept the eating habits of our ancestors, who evolved to get the most nutrition from the food they ate, but our lifestyle today is totally different from our ancestors,” says Wang.  “In the 21st century we need a new way of thinking.”

 

Published May 2009

###

1Volkow N. Issues for DSM-V: Should Obesity Be Included as a Brain Disorder? Am J Psychiatry 2007 May; 164(5):708-710.

2Wang GJ et al.  Exposure to appetitive food stimuli markedly activates the human brain. NeuroImage 2004; 42:1515-1537.

3Wang GJ et al.  Evidence of gender differences in the ability to inhibit brain activation elicited by food stimulation.  Proceedings of the National Academy of Science 2009 January 27; 106(4):1249-1254.