Shared Perspectives

Although important advances have been made regarding the etiology, prevention and treatment of anorexia nervosa, bulimia nervosa and binge-eating disorder, obesity has received less attention from researchers and clinicians in the eating disorders field. This is unfortunate for two reasons.

First, obesity accounts for far more morbidity and mortality than all the eating disorders combined because it is much more prevalent and is associated with serious health problems (diabetes, coronary heart disease, cerebrovascular disease, colorectal cancer). Currently, 30 percent of Americans are obese, compared with the 4 percent who meet criteria for anorexia nervosa, bulimia nervosa, or binge-eating disorder. Indeed, obesity is credited for approximately 300,000 deaths annually in the United States alone, making obesity the second most prevalent preventable cause of death.

Second, it is probable that there is overlap between the risk factors for obesity and those for bulimia nervosa and binge-eating disorder because all three involve caloric overconsumption. One implication of this possibility is that prevention and treatment programs might be able to reduce both eating disorders and obesity.


The neglect of obesity by the eating-disorders community may be the result of two factors. First, obesity is not considered a psychiatric disorder. This may be interpreted to suggest that obesity is not a disorder of eating. There is now incontrovertible experimental evidence indicating that body mass is a direct function of caloric intake relative to caloric expenditure (the energy equation). Research has also documented that obese individuals consume more calories and exercise less than their lean counterparts (dispelling the myth that obese individuals do not consume more calories). It seems reasonable to consider that a medical condition caused by excessive eating, relative to caloric needs, is a disorder of eating.

Many individuals ascribe much import to genetic factors in explaining the etiology of obesity. However, the fact that the rates of obesity have gone from 4 percent to 30 percent during the last century suggests that genetic effects are be-haviorally mediated (genes do not change this quickly). That is, the most plausible explanation for the exponential increase in obesity is unhealthy lifestyle--we are consuming more calories than is warranted given our sedentary lifestyle. This analysis should be viewed with optimism. If we change our lifestyle so that there is equilibrium between caloric intake and output, we should be able to dramatically reduce the rates of obesity and the consequent morbidity and mortality.

A second factor that may have discouraged the eating-disorders community from focusing on obesity is the belief that dieting causes eating disorders. This places researchers and clinicians in a conundrum because they fear they will increase the risk for eating disorders if they promote a reduction in caloric overconsumption. Fortunately, recent experimental data indicate that placing people on a caloric deficit diet (if they are overweight) or a caloric-balanced diet (if they are not yet overweight) actually decreases binge eating and bulimic pathology. To date, there are no experimental data that indicate that dieting increases the risk for onset of exacerbation of eating pathology--rather, it seems to reduce eating disturbances.


The eating-disorders community should focus greater research and clinical attention on obesity. There are a number of important gaps in our knowledge regarding the etiology, prevention and treatment of obesity. First, additional research is needed on the risk factors for onset of obesity. What are the foods that most increase risk for weight gain? What are the shared risk factors for both obesity and eating pathology? Second, prevention programs that target both of these adverse outcomes should be developed and evaluated.

The focus on prevention efforts is particularly important because most individuals have an incredibly difficult time losing weight and maintaining this reduced weight once they have become obese. There is also evidence that there are biological changes that occur with a high-fat diet that may make it more difficult to subsequently switch to a low-fat diet (e.g., receptor upgrading for the opiate effects of certain high-fat foods). Finally, treatment programs for eating disorders should incorporate a stronger emphasis on promoting a healthy lifestyle that helps patients approximate a healthier body mass.

Eric Stice is an assistant professor of psychology and eating disorders researcher at the University of Texas at Austin.