with eating disorders are in need of critical examination, as such agents are commonly employed despite the current absence of evidence of efficacy.

Because eating disorders are uncommon, multisite studies will be necessary for the definitive examination of treatment efficacy and of relapse prevention. Multisite studies will further support initiatives to establish standards for terminology and assessment, as standardization is required for the execution of such trials. Another significant advantage of multisite studies is that the enhanced power will provide the opportunity to conduct more specific investigations of the relationship between eating disorder subtype, comorbidity, treatment response, and relapse.

In addition, novel approaches to study design and procedures in the treatment of adolescents with eating disorders should be considered not only for developmental considerations in treating younger patients but also because many eating disorder research centers serve as secondary and tertiary referral centers and therefore do not currently treat significant numbers of younger, new-onset cases. The particular ethical considerations and the reluctance of parents to have their children participate in clinical research are also critical issues that need to be addressed to increase clinical research initiatives focused on adolescents with eating disorders.

While there have been numerous studies to identify risk factors for the development of anorexia nervosa, few true risk or protective factors for the development of anorexia nervosa have been definitively established. Population-based longitudinal databases, which include prospectively collected data on large populations that include incident cases, may shed light on questions of etiological relevance to anorexia nervosa. Such projects must be viewed as a priority. Research on the risk factors for anorexia nervosa must be appropriately divided between biological–genetic and environmental factors. Because anorexia nervosa is influenced by both biological and en vironmental factors, a comprehensive exploration of gene and environment interactions may provide valuable information about the etiology of this disorder.

Factors such as perceived pressure to be thin, thin-ideal internalization, body dissatisfaction, and negative affect have been identified as risk factors for the development of bulimia nervosa. Future research should be directed at identifying new risk factors for bulimia nervosa, as most of the established risk factors have relatively modest effect sizes (Stice, 2002). Promising variables include hypersensitivity to negative interpersonal transactions, cognitive factors (e.g., affect regulation expectancies), feeding avidity, and individual differences in reinforcement from eating. In addition, the role of dieting in the development of bulimic pathology should be clarified.

Research should also begin to examine potential biological risk factors for bulimic pathology (e.g., serotonin abnormalities and structural differences in the orbitofrontal cortex); research has yet to identify a single biological risk factor for bulimic pathology. Furthermore, studies should continue to search for genetic factors that influence risk for this eating disorder.

Relatively little is known about the ways in which risk factors work together to promote the development of this disorder or about possibly distinct etiologic pathways in bulimia nervosa. Thus future research should test multivariate models to determine how the various risk factors work in concert to promote bulimic pathology. It will be particularly important to focus greater attention on identifying protective and potentiating factors and on the means by which psychosocial and biological factors work together to foster bulimic pathology.

Research should also investigate whether the risk factors for symptom onset differ from those for symptom escalation and maintenance. This is important because the former are germane to the design of universal and selected prevention programs, but the latter are necessary for the design of optimally effective indicated prevention programs and treatment interventions.

More generally, the use of prospective and experimental designs should be encouraged. These research methods are potentially powerful means of elucidating the etiologic processes that give rise to eating disorders.

Research on professionally administered weight loss programs for overweight children and adolescents indicates that these programs do not appear to increase symptoms of eating disorders. Conclusions about the relationship between the treatment of obesity and eating disorders are based on a very limited number of studies, and further research is needed before firm conclusions can be reached. In particular, studies are needed to reconcile findings of the apparently benign effects of dieting, as practiced in behavioral weight loss programs, to determine whether dieting precipitates eating disorders. Several issues must be considered.

First, healthy dieting, which encourages only modest caloric restriction, in combination with increased consumption of low-fat dairy products and fruits and vegetables, appears to present few risks to overweight youth. As previously mentioned, this type of dieting is likely to improve the nutritional value of foods consumed. By contrast, unhealthy weight loss behaviors, which include severe caloric restriction (e.g., crash diets) and the prohibition of certain foods (e.g., fad diets), could significantly increase the risk of eating disorders and emotional complications. This is possible in overweight youth, as well as in normal-weight girls who diet aggressively in pursuit of an ever-thinner ideal. Similarly, chronic restrained eating may pose risks that are not associated with healthy dieting.

Second, disturbances in eating behavior and mood must be clearly defined and measured. The pediatric obesity studies reviewed in this volume did not assess criteria for the diagnosis of bulimia nervosa, binge eating disorder, or eating disorder not otherwise specified. None, for example, measured objective or subjective binge episodes, as defined by Fairburn and Cooper (1993). Future studies could incorporate efforts to modify the Eating Disorder Examination (Fairburn & Cooper, 1993) for use with children and adolescents (Bryant-Waugh, Cooper, Taylor, and Lask, 1996).

Third, some overweight youth may be at greater risk for adverse behavioral consequences of dieting and weight loss, even when they participate in a professionally administered program. Longitudinal studies, for example, have shown that severe body image dissatisfaction and weight and shape preoccupation are the most robust predictors of the development of eating disorders in adolescent girls. Thus, overweight teenagers with marked body image dissatisfaction, depression, or other psychiatric complications may be at greatest risk of experiencing binge eating episodes when subjected to even modest caloric restriction, and research in this area is needed.

Finally, weight regain is common in overweight adolescents, as in obese adults. Studies of adults have not found weight cycling (i.e., weight loss followed by regain) to be associated with clinically significant behavioral consequences; however, in overweight youth with a history of psychiatric complications, weight cycling might produce different effects. Whenever possible, follow-up assessment should be conducted through late adolescence when symptoms of bulimia nervosa or binge eating disorder might emerge.

Ultimately, large-scale randomized controlled trials will be needed to determine the behavioral risks posed by different weight loss interventions for overweight youth. Ethical constraints will limit investigators from using such trials to assess the effects of crash diets and other fundamentally unsound approaches. In addition, given the generally low occurrence of eating disorders, case–control studies may provide a better mechanism of identifying dietary practices most likely to be associated with adverse behavioral effects. Health professionals, teachers, and parents will continue to be concerned about misguided weight loss efforts in children and teenagers, but all should be increasingly concerned about the growing epidemic of pediatric obesity. Fifteen percent of America's adolescents are already overweight and as adults will experience serious medical and psychosocial consequences of this condition. Concerns about potential ill

effects of dieting should not impede efforts to improve the treatment of pediatric obesity. More important, such concerns should not discourage urgently needed efforts to prevent the development of overweight in both children and adults.

Prevention research is an important issue in eating disorder research, even though the impact of eating disorder prevention programs for children and adolescents is not clear (Pratt & Woolfenden, 2002). Future research should include longitudinal studies of universal prevention with an integrated, multidimensional, and systemic approach to schools and other important parts of the community. These studies should demonstrate significant reductions in risk factors and a reduction in incidence of the disorders. In addition, studies of targeted interventions are needed to focus on valid and ethical ways to identify individuals and environments that are at-risk and provide interventions that reduce risk factors and incidence of the disorders. Research should demonstrate that significant and important changes in the putative risk factors or protective factors can be achieved and maintained.