Objective: Although binge eating disorder is a common and distressing concomitant of obesity, it has not yet been established whether affected individuals presenting to behavioral weight control programs should receive specialized treatments to supplement standard treatment. This study was designed to examine the added benefit of two adjunctive interventions, individual cognitive behavioral therapy (CBT) and fluoxetine, offered in the context of group behavioral weight control treatment.Research Methods and Procedures: One hundred sixteen overweight/obese women and men with binge eating disorder were all assigned to receive a 16‐session group behavioral weight control treatment over 20 weeks. Simultaneously, subjects were randomly assigned to receive CBT + fluoxetine, CBT + placebo, fluoxetine, or placebo in a two‐by‐two factorial design. Outcome measures, assessed at the end of the 16‐session acute treatment phase, included binge frequency, weight, and measures of eating‐related and general psychopathology.Results: Overall, subjects showed substantial improvement in binge eating and both general and eating‐related psychopathology, but little weight loss. Subjects who received individual CBT improved more in binge frequency than did those not receiving CBT (p< 0.001), and binge abstinence was significantly more common in subjects receiving CBT vs. those who did not (62% vs. 33%,p< 0.001). Fluoxetine treatment was associated with greater reduction in depressive symptoms (p< 0.05). The 54 subjects who achieved binge abstinence improved more on all measures than the 62 subjects who did not. In particular, these subjects lost, on average, 6.2 kg compared with a gain of 0.7 kg among non‐abstainers.Discussion: Adjunctive individual CBT results in significant additional binge reduction in obese binge eaters receiving standard behavioral weight control treatment.

This study was designed to investigate the biological underpinnings of the observed deficit in satiety in patients with bulimia nervosa. Eight women with bulimia nervosa and 10 age- and weight-matched control subjects consumed three laboratory meals consisting of 200, 400, and 600 g of a radiolabeled liquid meal. For 1 h after each meal, blood samples were obtained at 10-min intervals for measurement of cholecystokinin concentration and gastric emptying was measured. Subjects also completed perceptual rating scales at 10-min intervals. Compared with control subjects, patients with bulimia nervosa showed a blunting of postprandial cholecystokinin release, particularly with larger meal sizes, as well as delayed gastric emptying. Increasing meal size was associated with increased desire to binge eat in patients but not in control subjects. These data lend support to a model in which increased gastric capacity, perhaps resulting from repeated binge eating, gives rise to delayed gastric emptying and blunted postprandial cholecystokinin release, leading to an impaired satiety response, which tends to perpetuate the illness.