مدل یادگیری پرخوری: واکنش پذیری نشانه و مواجهه با نشانه
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|39009||1998||16 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Behaviour Research and Therapy, Volume 36, Issue 3, March 1998, Pages 257–272
Abstract In the present article, a learning model of binge eating is presented. It has been hypothesized that, parallel to drug intake, the craving and excessive food intake of binge eaters is cue controlled. Research in support of the model is reviewed and a series of predictions about clinical and non-clinical issues is derived from the model. Amongst other things, the model predicts that binge eating might be successfully treated with cue exposure and response prevention. Practical issues are discussed and preliminary pilot studies on cue exposure for bingers are reviewed.
نتیجه گیری انگلیسی
Concluding remarks The present learning model of binge eating states that cues which reliably signal food intake, such as the sight, smell and taste of food, may start to act as conditioned stimuli which trigger cue reactivity or conditioned responses. It is assumed that learned cue reactivity, e.g. the autonomic or biochemical responding and craving, increases the probability of (excessive) food intake. Findings on the eating behavior of binge eaters indirectly support the classical conditioning model of binge eating and also in line with the model is the eating behavior of restrained eaters, who are considered to be an analogue sample of binge eaters. Bingers as well as restrained eaters have repeatedly been found to overeat after exposure to cues predicting intake, such as tasting a priming dose, the smell of binge food or thinking of binge food. It is hypothesized that these disinhibitors all act as conditioned stimuli with an identical consequence: binge eating. The CSs are assumed to elicit cue reactivity (autonomic and/or biochemical responses which are subjectively experienced as craving) and, therefore, lead to binge eating. Final evaluation of the model must, however, await studies which test the central predictions that follow directly from the model. Although there have been a number of small-scale, primarily uncontrolled short-term studies that suggest that cue exposure is an effective therapy for binge eating, for the time being there are two reasons why it should not be applied as the sole type of treatment. To begin with, there are no properly controlled data about the effectiveness of the treatment on either the short or long term. Pilot studies suggest that cue exposure is an extremely effective method for combating binges, but this must as yet be confirmed through properly controlled, large-scale studies. Secondly, and certainly equally important, is the fact that most binge eaters not only suffer from binge eating: they attempt to prevent their weight from increasing through bizarre methods (such as not eating for days, intentionally regurgitating and using laxatives), have a low self-esteem and their way of thinking about their body weight and shape is dysfunctional. Whether these symptoms can be favorably influenced through cue exposure remains to be seen. Studies on the effectiveness of cue exposure should therefore measure all relevant symptoms, including general psychopathology, eating pattern, weight control methods, self-esteem as well as body weight and shape concern. However, we do not recommend that cue exposure be combined with antidepressants which reduce bingeing urges, such as serotonergic reuptake inhibitors. These medicines probably reduce the cue reactivity, making sufficient extinction impossible. We would also discourage subjecting anorexia nervosa and other underweight patients to cue exposure. For these patients, binges are often their only remaining source of energy. If this source dries out, their ultimate objective of not eating at all will have been achieved. An anorexic patient can be given the promise of an effective treatment against bingeing once she is “back to weight”. Note that, in case of bulimia nervosa, a similar danger exists. Patients with bulimia nervosa are really “failed anorectics”: they would love to be skin over bones and not suffer from bingeing. It is conceivable that cue exposure will help the patient to exchange her bulimic straitjacket for an anorexic one. Jansen et al. (1992)demonstrated an increase in restrained eating after successful exposures. For the time being, we recommend that therapists combine cue exposure with interventions aimed at the normalisation of eating behavior and dysfunctional cognitions. One might think of adding the diet management and cognitive elements from Fairburn’s cognitive behaviour therapy—of which the effectiveness has been sufficiently proven (see Fairburn et al., 1995), but it might also be an interesting enterprise to combine cue exposure with Rosen’s new and promising body image therapy. Rosen’s body image therapy includes cognitive restructuring of dysfunctional cognitions concerning body shape and weight as well as gradual exposure to a hierarchy of distressing aspects of appearance and the prevention of body checking behavior. The combination of both new and promising methods, cue exposure and body image therapy, directly focuses at the two main symptoms of bulimia nervosa: binge eating (combating with cue exposure) and dysfunctional cognitions concerning body shape and weight (combating with body image therapy) and thus might be a very effective cognitive behavior therapy. Only research can tell.