Everyone seems to know individuals who binge eat, yet stay lean and conversely, individuals who ingest less than a thousand calories a day yet are obese. Scientists believe they are on the cusp of identifying how genetic and neurochemical processes produce a variety of eating disorders.
The findings may lead to the creation of new, targeted drug therapies including preventative measures and treatment strategies for people with binge-eating disorders and obesity.
University of Alabama at Birmingham (UAB) psychologist Mary Boggiano, Ph.D. and colleagues developed an animal model for binge eating disorder, which affects an estimated one in 20 Americans. From the model, UAB psychologists hope to determine the genetic and neurochemical differences that characterize lean from obese binge eaters and obese individuals who don’t binge.
In the study, published in the April 2007 issue of the International Journal of Obesity, UAB psychologists identified rats who are predisposed to binge on large quantities of palatable food – sugary and high-fat junk foods – in a short period of time. Eating a large amount of palatable food in one sitting, however, did not predict susceptibility to become obese, just as some human binge eaters become obese while others remain lean.
Although binge eating disorder is the most common of all eating disorders, affecting 5 percent of the U.S. population, it does not have a formal mental health diagnosis due to a lack of research. Obesity and binge-eating disorders such as bulimia and binge-purge anorexia affect 40 percent of the population. But often patients are given the same set of treatments regardless of the condition or disorder.
Boggiano assigned rats as “binge prone” or “binge resistant” based on the amount of palatable food, (Oreo® cookies), they consistently ate when given a choice between the cookies and regular chow. When only chow was offered, none differed in their intake of chow, but when cookies were presented, the rats ate more cookies. The binge-prone groups’ penchant for junk food may be driven by taste rather than by a preference for any one macronutrient, such as carbohydrates or fats, since they also ate more Froot Loops® and Crisco®, which do not contain any fat or carbohydrate, respectively.
To the psychologists’ surprise, the amount of junk food the rats ate, whether binge prone or binge resistant, was not predictive of whether the rats became obese. In fact, obesity and obesity resistance was equally represented in both the binge prone and binge resistant groups.
The finding is consistent with humans in that not everyone who frequently craves or eats junk food is obese. The lean binge-prone group resembles bulimia nervosa patients who generally do not gain weight, while the binge-prone obese group parallels patients who binge and gain weight, typical of binge-eating disorder. The binge-resistant obese group mirrors two-thirds of the obese population who consume a high number of calories but do not binge.
One finding was that if the rats were given a daily diet of chow and cookies, both groups regulated their intake of Oreo® cookies and did not become obese the way half of the rats did when they were put on a high-fat, but nutritious diet. This may mean that it is easier to control caloric intake with low-fat meals and occasional junk snacks than with high fat meals, Boggiano said.
Another finding was that when under stress, the binge-prone rats ate less chow while the binge resistant rats ate less of the palatable junk food. The hesitation of binge prone rats to forsake palatable junk food may be mediated by the same mechanisms that cause binge eaters to seek out junk food when stressed or when experiencing negative emotions, Boggiano said.
The study argues against the notion that because animals lack higher cognitive processes, they cannot be used to help researchers understand complex behaviors such as binge eating and overeating that lead to obesity in humans, Boggiano said.