Elsevier

Appetite

Volume 55, Issue 3, December 2010, Pages 734-737
Appetite

Short communication
The study of food addiction using animal models of binge eating

https://doi.org/10.1016/j.appet.2010.09.010Get rights and content

Abstract

This review summarizes evidence of “food addiction” using animal models of binge eating. In our model of sucrose bingeing, behavioral components of addiction are demonstrated and related to neurochemical changes that also occur with addictive drugs. Evidence supports the hypothesis that rats can become dependent and “addicted” to sucrose. Results obtained when animals binge on other palatable foods, including a fat-rich food, are described and suggest that increased body weight can occur. However, the characterization of an addiction-like behavioral profile in animals with binge access to fat requires further exploration in order to dissociate the effect of increased body weight from the diet or schedule of feeding.

Section snippets

The concept of food addiction

As reported at the Columbia University Seminar on Appetitive Behavior, the obesity epidemic has various proposed causes, one of which is the concept of “food addiction.” This theory posits that people can become addicted to food, in ways similar to how some people are addicted to drugs. It is thought that food addiction can lead to overeating, which can result in increased body weight or obesity in select individuals. Stories of “food addiction,” particularly “sugar addiction,” abound in the

Modeling food addiction in laboratory animals: a focus on binge eating

Laboratory animal models have been used to study food addiction. Beginning in Bart Hoebel's laboratory, we adapted models that were developed with rats for studying drug dependence to test for signs of food dependence, with the eventual goal of identifying the neurochemistry associated with these behaviors. Addiction in humans is a complex disorder; for simplicity it is discussed in three stages (American Psychiatric Association, 2000, Koob and Le Moal, 1997). Bingeing is defined as a bout of

An animal model of sugar bingeing

Our most studied model is that of sucrose bingeing. In this model, rats are maintained on a diet of 12-h access to a 10% sucrose solution (or 25% glucose in earlier studies) and standard rodent chow, followed by 12-h of sucrose and chow deprivation, for about one month. We have published extensively using this model and relating it to a variety of factors associated with addictive behavior. What follows is a summary of those findings (also see Table 1); details can be found in our review papers

Bingeing on a fat-rich food

As noted above, rats bingeing on sucrose do not gain excess body weight, suggesting that sucrose bingeing might foster characteristics of addiction, but it alone is probably not responsible for obesity or weight gain. However, we have shown that when a highly palatable combination of sugar and fat is offered to rats, it instigates binge eating and also increases body weight (Berner, Avena, & Hoebel, 2008). We reduced the duration of palatable food access from 12 to 2 h in order to make the binge

Summary and conclusions

The models of binge eating in rats described herein provide tools with which to study the concept of food addiction and its resultant neurochemistry. The data suggest that binge intake of sugar can have dopaminergic, cholinergic and opioid effects that are similar to those seen in response to some drugs of abuse, albeit smaller in magnitude. Newer data generated from studies of bingeing on a sweet-fat chow show that it produces increased body weight, providing a potential link to obesity. These

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      Citation Excerpt :

      The study supports the that there could be an addiction to sucrose as a food ingredient. Additionally, obtained results showed that bingeing on other palatable foods, including a fat-rich food, causes increased body weight (Avena, 2010). The association between food addiction and substance abuse has been applied to the YFAS (Gearhardt et al., 2016) using the criteria in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V) Vahia, 2013.

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    Based on a presentation by Nicole Avena at the Columbia University Seminar on Appetitive Behavior. September 17, 2009, Harry R. Kissileff, Chairman, supported in part by GlaxoSmithKline and The New York Obesity Research Center, St. Luke's/Roosevelt Hospital. This research was supported by USPHS grants DK-079793 (NMA), MH-65024 (Bartley G. Hoebel), and AA-12882 (BGH). Appreciation is extended to Dr. Bart Hoebel and Miriam Bocarsly for their suggestions on the manuscript.

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