Kimberly D. Oswald

Incidence of chaotic eating Behaviors in binge-eating disorder: Contributing factors

Abstract Because dieting is not as common in patients with binge-eating disorder (BED) as among patients with bulimia or anorexia nervosa, the authors assessed the incidence, frequency, and contributing factors of semistarvation-like eating patterns in BED patients in this study, the first to explore such behaviors in a clinical population. They administered the Semistarvation-Associated Behaviors Scale (SSABS) to 54 women seeking BED treatment and to 29 controls. The aberrant eating behaviors among BED clients were associated with current dieting and certain BED criteria, (p < .05). The strongest contributor to chaotic eating patterns was negative affect preceding BED (r - .45, p < .001). This finding highlights the behavioral psychopathology of BED and strengthens the role of negative affect in precipitating binge episodes associated with the disorder. These behaviors may help maintain BED by creating a binge-negative affect cycle. The SSABS is a tool that may help break this cycle.

Body composition and endocrine status of long-term stress-induced binge-eating rats

Clinical binge eating runs a protracted course. The etiology of binge eating remains perplexing in part because, in humans, it is difficult to isolate and assess the independent and aggregate impact of various contributing variables. Using rats, we found that footshock stress and a history of caloric restriction (S+R), combine synergistically to induce binge eating. Stress and dieting are also strong antecedents and relapse factors in human eating disorders. Here we report further behavioral and physiological parallels to human binge eating. Like the protracted course of human binge eating, young female Sprague-Dawley rats continued to binge eat after 23 restriction/stress cycles (7 months) and this despite experiencing no significant weight loss during the restriction phases. Stress alone reduced adiposity by 35% (p<0.001) but S+R rats had no significant fat loss. An endocrine profile of normal plasma leptin and insulin levels but marked elevation of plasma corticosterone levels was found only in the binge-eating (S+R) rats (p<0.01), also paralleling endocrine profiles reported in clinical binge-eating studies. These behavioral and physiological similarities between this animal model and clinical binge eating increase its utility in understanding binge eating. Importantly, our findings also highlight the stubborn nature of binge eating: once a critical experience with dieting and stress is experienced, little if any further weight loss or food restriction is necessary to sustain it.

Family Caregivers of Women with Physical Disabilities

Cross-sectional, correlational analyses of data from two separate studies were conducted to examine the correlates of adjustment among family caregivers of women with disabilities. Participants included 40 caregivers of women with spinal cord injuries in the first study and 53 caregivers of women with cerebral palsy, traumatic brain injury, and other neuromuscular disabilities in the second study. It was hypothesized that a negative problem-solving style would be associated with greater caregiver distress in both studies, and that caregiver adjustment would be associated with care recipient depression in the second study. As expected, results indicated that a higher negative orientation toward solving problems was associated with caregiver depression and lower well-being. However, in the second study, caregiver characteristics were not associated with care recipient depression. These data indicate that considerable variability exists in caregiver adjustment. Methodological limitations and the implications for research, service, and policy formation are! discussed.

Feeding response to melanocortin agonist predicts preference for and obesity from a high-fat diet.

Overconsumption and increased selection of high fat (HF) foods contribute to the development of common obesity. Because the hypothalamic melanocortin (MC) system plays an integral role in the regulation of food intake and dietary choice, we tested the hypothesis that proneness (-P) or resistance (-R) to dietary-induced obesity (DIO) may be due to differences in MC function. We found that prior to developing obesity and while still maintained on chow, acute, central administration of MTII, an MC agonist, produced a greater anorectic response in DIO-P rats than in DIO-R rats. However, after only 5 days of exclusive HF feeding, the DIO-R rats had significantly greater suppression of intake after MTII treatment than they did when maintained on chow. In addition, the DIO-P rats were much less responsive to MTII treatment than the DIO-R rats after only 5 days of the HF diet. In fact, MTII-induced anorexia during HF feeding correlated negatively with body weight gained on the HF diet. These results suggest that the voluntary decrease of HF feeding in DIO-R rats may be mediated by increased endogenous MC signaling, a signal likely compromised in DIO-P rats. Differences in MC regulation may also explain the observed preference for HF over a lower fat food choice in DIO-P rats. Finally, the results indicate that responses to exogenous MC challenge can be used to predict proneness or resistance to DIO.

Change in CCK-8 response after diet-induced obesity and MC3/4-receptor blockade.

Little is known regarding satiety effects of systemically administered cholecystokinin (CCK-8) in propensity or resistance to dietary-induced obesity (DIO), and of its effect under conditions of melanocortin-3/4R blockade. We found that CCK-8 exerted greater satiety effects in DIO-prone but not DIO-resistant rats, and this occurred only when the rats were placed on a high-fat (HF) diet, when DIO-prone rats failed to compensate for the greater energy density of the diet. CCK-8 also suppressed intake stimulated by melanocortin-3/4R antagonist, SHU9119, but only after 24h of increased feeding. This suggests that under both of these conditions, responsiveness to CCKs satiety effect is not so much affected by a HF diet or significant increases in body weight per se, but by a failure to rapidly limit food intake to that needed only for metabolic need. Identification of an early feeding mediator that is most strongly activated by a HF diet or by an acute challenge to energy homeostasis should provide an ideal anti-obesity target adjunct to CCK-8.