Individuals randomized to the Healthy Weight Program lost more weight over the intervention period than comparison controls (who gained weight over time), indicating that the intervention successfully manipulated weight-loss dieting. This weight loss effect highlights the primary difference between this intervention and CBT treatment, in that participants in the latter trials typically show a small increase in BMI by posttest (e.g., 0.9 BMI increase in Fairburn et al., 1991
, Fairburn, Jones et al., 1993
and Fairburn, Marcus et al., 1993
). However, in this trial, pretest to posttest decreased in BMI was relatively small (eta2
= .065 or r
= .26) and this effect faded by 3-month follow-up. The pattern of weight loss and regain observed in this trial is typical of most weight control interventions, wherein significant weight loss is not observed during the first few weeks, and maximum effects occur at posttest and fade over follow-up (Bennett, 1986
; Jeffery et al., 2000
). In fact, typical short-term low-calorie weight loss diets show similar small decreases in weight during a similar duration to this study (e.g., 0.21 decrease in BMI over 6-months of active treatment; Goodrick et al., 1998
). Furthermore, virtually all obesity treatment programs show an erosion of effects after termination of treatment (Jeffery et al., 2000
; Kramer, Jeffery, Forster, & Snell, 1989
). These findings collectively suggest that it is extremely difficult to promote lasting healthy lifestyle changes, even in normal weight individuals, and casts doubt on the ability of this intervention to produce lasting weight-loss effects.
Nonetheless, as hypothesized, intervention participants demonstrated significantly greater reductions in bulimic symptoms, including both binge and purge frequencies, than controls throughout the study. The fact that such large decreases in bulimic symptoms were observed, and that the effects persisted to 3-month follow-up, suggests that the Healthy Weight Program may show promise as a treatment for bulimia nervosa. The pretest to posttest effects for binge eating and compensatory behaviors were large and medium in magnitude (r
= .50 and .34, respectively), whereas a CBT meta-analysis found that the average pre to post effect sizes for binge eating and compensatory behaviors were both large (r
= .55 and .61, respectively; Ghaderi & Andersson, 1999
). One key difference between the interventions, however, was that the Healthy Weight Program lasts only 6-sessions over 8-weeks in duration, compared to the standard 20-week, 20-session CBT protocol. The average per-session effect size for change in binge eating and compensatory behaviors is r
= .03 for both outcomes for CBT, whereas the comparable per session effects sizes are r
= .08 and .06 for these outcomes for the Healthy Weight intervention. The fact that the clinical yield per hour of intervention is higher for the Healthy Weight intervention suggests that an expansion of the intervention may produce larger overall effects. The 3-month follow-up remission rate of 35% for the Healthy Weight intervention also compares favorably to the 1-year remission rates observed for CBT of 29% (Agras et al., 2000
). Similarly, 29% of intervention participants in remission at T3 relapsed at T4, which is also comparable to relapse rates observed in CBT trials (e.g., 34% in Agras et al., 2000
). These considerations suggest that it might be worthwhile to continue to refine and evaluate this treatment in larger-scale efficacy trials.
It was also hypothesized that the Healthy Weight Program would produce decreases in health care utilization and increases in social functioning. Significant intervention effects were observed for frequency of health care use, suggesting that an added benefit of this brief intervention is that it may reduce health care utilization and the associated costs. Given the high cost of health care, it is possible that the savings in health care costs may offset the expense of delivering this brief treatment. One possible explanation for the fact that the social function effects were only marginally significant is that improvements in social functioning may require a longer amount of time to develop, perhaps in part due to the nature of complex social relationships. Indeed, it has been hypothesized that improvements in social functioning are a secondary effect of treatment, and one that is not observed in some clinical trials until closer to 1-year follow-up (Fairburn, Jones et al., 1993
It was noteworthy that the attrition rate for intervention participants in this trial (28%) was similar to rates observed in previous clinical trials of CBT (27%; Agras et al., 2000
). Despite the shorter treatment duration, nearly one in three intervention participants withdrew from the study. This robust pattern of attrition may suggest that one-third of patients presenting for eating disorder treatment are actually ambivalent about treatment, regardless of form or content. In general, though many bulimic individuals may be distressed by their binge and purge routines and choose to seek treatment, they may also derive pleasure to their ability to binge-eat high fat and sugar foods without marked weight gain. The positive reinforcement attained from binge eating, for some individuals, may then outweigh the perceived benefits of treatment, thus resulting in a subset of treatment participants who are not willing to relinquish their disordered behaviors.
This trial also provided a unique opportunity to examine the role of dieting in the maintenance of bulimic symptoms. Intervention participants successfully lost weight during the intervention and evidenced significant decreases in binge eating and compensatory behaviors compared to controls. Remarkably, this current study represents the seventh experimental study of the effects of confirmed weight loss or weight maintenance diets on bulimic symptoms. Five other randomized clinical trials have found that assignment to low-calorie weight loss diets results in significantly greater decreases in binge eating and bulimic symptoms for normal weight, overweight, and obese adolescent and adult women relative to waitlist controls (Goodrick et al., 1998
; Groesz & Stice, 2005
; Klem et al., 1997
; Presnell & Stice, 2003
; Reeves et al., 2001
). Assignment to a more moderate weight-maintenance diet similarly decreased bulimic symptoms over the course of a year in normal weight adolescents compared to waitlist controls (Stice, Presnell et al., 2005
). To the best of our knowledge, no experimental study that has manipulated dieting has provided support for the dietary restraint model of bulimic pathology. Furthermore, the current study is a unique addition, which illustrates that even a clinical population of individuals with bulimia nervosa demonstrates reductions in bulimic behaviors when encouraged to engage in a moderate weight-loss diet.
Collectively, these findings raise serious questions about the role of dieting in the maintenance of bulimic pathology. Though it is possible that dieting is a proxy risk factor, not a direct contributor to the development of bulimia nervosa, it appears unlikely that attempts to achieve a negative energy balance, per se, are maintaining bulimic symptoms. Furthermore, a recent study also suggests that participants in a weight maintenance diet show lower rates of binge eating and compensatory behavior onset than assessment-only controls (Stice, Shaw, Burton, & Wade, in press
), which raises the possibility that the role of dieting in the onset of bulimic symptoms may be suspect as well.
The most likely reason for the discrepancy between longitudinal studies indicating that dieting predicts onset of bulimic symptoms and experimental treatment trials indicating that assignment to weight loss diets decease bulimic symptoms is that the self-report measures of dieting used in the former studies are invalid. Research has found that dietary restraint scales do not show a significant or substantively meaningful inverse correlation with objective measures of acute or chronic caloric intake (Bathalon et al., 2000
; Stice et al., 2004
), as was suggested by the original validity studies that relied on self-reported caloric intake. In addition, individuals with elevated scores on dietary restraint scales tend to gain significantly more weight over both short and long periods of time relative to their lower-scoring counterparts (French, Jeffery, & Wing, 1994
; Klesges et al., 1989
; Klesges et al., 1992
; Stice, 2001
; Stice et al., 1999
), providing further evidence that they are not entering a lasting state of negative energy balance.
If this assertion is true, it is possible that dieting has been falsely implicated as a risk and maintenance factor for bulimic pathology. Alternative treatments that do not target dieting (e.g., IPT and DBT) also show promise for treating this disorder, and results from the present trial demonstrate that promoting a negative energy balance can successfully reduce bulimic symptoms in a clinical population. These collective findings suggest that factors other than dietary restraint might be maintaining bulimia nervosa. Perhaps the effects from CBT may come primarily from its focus on weight and shape overvaluation, or perhaps both the CBT and Healthy Weight Program effects stem from the fact that both interventions promote healthy dieting and healthy eating strategies, albeit in different ways. It is also possible that participant expectancies, demand characteristics, or attention account for effects across all treatments, which suggests that future placebo-controlled trials are warranted to rule out this possibility. Future replication is also certainly indicated, but initial findings from this study appear incompatible with the notion that dieting is a principal factor in the maintenance of bulimia nervosa.
First, the present study compared an active intervention to a waitlist control, but did not utilize a placebo control group. Although comparison to waitlist allowed for the ability to rule out regression to the mean, passage of time, and measurement-artifact alternative explanations for the effects of the intervention, a placebo comparison group has the added advantage to rule out the possibility that intervention effects resulted from expectancy effects, demand characteristics, or attention. In this first study we thought it best to utilize a standard control group to facilitate comparison of results from this study to those of past trials. Indeed, past psychosocial treatment trials for eating disorders have almost exclusively compared active interventions to waitlist control groups instead of placebo or alternative intervention control groups. Nevertheless, the development of an equally credible placebo control that controls for time, dosage, and attention effects would significantly benefit all clinical trials in this field. Second, the present study only used a 3-month follow-up. It would have been preferable to follow participants much longer, and track treatment effects in regular intervals throughout. Third, with the exception of direct measures of height and weight, we relied solely on self-report data in this trial. In the future, it would be preferable to, whenever possible, collect multiple-informant data and objective behavioral data. Fourth, the moderate sample size limited our power to detect intervention effects. Though we had adequate power (>.82) to detect medium effect sizes (r
= .30; Cohen, 1988
), effects that were smaller in magnitude may have been missed.