Can Obesity Be an Addiction?

Bret S. Stetka, MD; Nora D. Volkow, MD

Disclosures

July 16, 2013

In This Article

Editor's Note: In June 2013, the American Medical Association (AMA) declared obesity a disease, a move championed by many clinicians and derided by others. Debate aside, the announcement reinforced that the understanding and appreciation of obesity is evolving, and that in this era of soda bans and school lunch reform, obesity is high in the consciousness of both the public and the medical community.

One area of obesity research receiving a great deal of attention lately is the considerable neurobiological overlap between addiction and some forms of obesity. Nora D. Volkow, MD, Director of the National Institute on Drug Abuse (NIDA), has studied this association extensively. Medscape recently spoke to Dr. Volkow about her ongoing research into the relationship between weight and addiction.

Obesity and Addiction: Introduction

Medscape: Hi, Dr. Volkow. Before we get to the relationship between obesity and addiction, how does human appetite control normally work?

Dr. Volkow: Eating behaviors are obviously necessary for survival, and we've evolved complex and redundant systems to ensure that the behaviors necessary to eat occur. The brain receives peripheral signals that relate to the body's nutritional status: for example, the concentration of glucose, lipids, and certain nutrients. These signals are conveyed to the brain via the plasma and peripheral nerves in the gastrointestinal tract -- a process known as "homeostatic regulation" of feeding -- and help indicate whether the body needs to consume more food or not and whether there is a need for a specific nutrient. Parallel reward systems in the brain respond to the pleasantness of food and motivate our behaviors to consume them, a process described as "hedonic regulation" of food intake.

It was believed for many years that these peripheral signals were predominantly received by the hypothalamus, and it was initially thought that there were only a few signals (eg, glucose, insulin, leptin). However, in the past 10 years, many other signals (eg, hormones, peptides) have been identified that work in part by acting on and altering the sensitivity of reward systems in the brain to food.

For example, normally the hormone leptin is secreted from adipose cells to tell the brain that enough energy is stored; this decreases appetite and increases energy expenditure. There is a very rare genetic condition where individuals are born without the gene that encodes for leptin, and these individuals overeat and become obese from childhood. In these individuals, brain imaging studies have shown that reward systems in the brain are hypersensitive to the rewarding properties of food. Leptin treatment in these individuals decreases the sensitivity of the reward system, resulting in a decrease in the motivation to eat and a marked reduction in weight.

When peripheral signals -- such as leptin or insulin -- are not released, or your brain becomes tolerant to them, you don't have a mechanism to counter the drive to eat. It's like driving a car without brakes.

Medscape: Which brain regions make up our reward centers?

Dr. Volkow: We describe them as a reward circuit, because there are multiple connected regions involved. A central node in the circuit is the nucleus accumbens (NAc), a region regulated by dopamine, which we always hear about being responsible for the rewarding and addictive effects of drugs. The rewarding effects of drugs result from their ability to activate the NAc through increased dopamine release. Similarly, rewarding effects of food are linked to dopamine release in the NAc.

Before we get to food addiction, I should say that how effective food is at activating these dopamine pathways, and the NAc, is modulated by homeostatic peripheral signals. If you don't have insulin and leptin, which decrease dopamine signaling in the NAc, the reward circuit will go into overdrive when you eat or are exposed to food; this is because signaling in the reward pathway triggers the motivation to eat. This can result in obesity. As people become obese, they become insulin- and leptin-resistant, thus removing the normal peripheral signals that help inhibit the rewarding effects of food; the more severe the obesity, the worse the brain becomes at preventing excess food intake.

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