Institutional members access full text with Ovid®

Share this article on:

Natural Addiction: A Behavioral and Circuit Model Based on Sugar Addiction in Rats

Hoebel, Bartley G. PhD; Avena, Nicole M. PhD; Bocarsly, Miriam E. BA; Rada, Pedro MD

Journal of Addiction Medicine: March 2009 - Volume 3 - Issue 1 - p 33-41
doi: 10.1097/ADM.0b013e31819aa621
Review Article

The distinction between natural addiction and drug addiction is interesting from many points of view, including scientific and medical perspectives. “Natural addictions” are those based on activation of a physiobehavioral system, such as the one that controls metabolism, foraging, and eating to achieve energy balance. “Drug addictions” activate many systems based on their pharmacology. This review discusses the following questions: (1) When does food produce a natural addiction? Sugar causes signs of addiction if the scheduling conditions are appropriate to cause binge eating. (2) Why does addictive-like behavior result? Bingeing on a 10% sucrose solution repeatedly releases dopamine in the nucleus accumbens, and it delays the release of acetylcholine, thereby postponing satiety. Opioid involvement is shown by withdrawal caused by naloxone or food deprivation. Bingeing, withdrawal, and abstinence-induced motivation are described as the basis for a vicious cycle leading to excessive eating. (3) Which foods can lead to natural addiction? A variety of sugars, saccharin, and sham feeding are compared with bingeing on high-fat diets, which seem to lack sugar’s opioid-withdrawal characteristic. (4) How does natural food addiction relate to obesity? Low basal dopamine may be a common factor, leading to “eating for dopamine.” (5) In a neural model, the accumbens is depicted as having separate GABA output pathways for approach and avoidance, both controlled by dopamine and acetylcholine. These outputs, in turn, control lateral hypothalamic glutamate release, which starts a meal, and GABA release, which stops it.

From the Department of Psychology and Princeton Neuroscience Institute (BGH, NMA, MEB), Princeton University, Princeton, NJ; The Rockefeller University (NMA), New York, NY; Department of Psychology (MEB), Princeton University, Princeton, NJ; and Department of Physiology (PR), University of Los Andes, Merida, Venezuela.

Received for publication October 31, 2008; accepted December 31, 2008.

Send correspondence and reprint requests to Dr. Bartley G. Hoebel, Princeton University, Department of Psychology, Washington Road, Princeton, NJ 08540. e-mail: hoebel@princeton.edu

Supported by USPHS Grants DA10608, MH65024, and AA12882 (to BGH) and fellowship DK-079793 (to NMA).

© 2009 American Society of Addiction Medicine