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This paper reviews research investigating the comorbidity between eating disorders and anxiety disorders. Whilst there is some inconsistency in the literature, it appears that women with eating disorders have higher rates of anxiety disorders than normal controls. Potential causal relationships between eating disorders and anxiety disorders are outlined, though their relative chronology appears to be somewhat inconsistent. Safety behaviours and cognitive avoidance strategies (i.e., cognitive narrowing and blocking) are suggested as potential mechanisms linking the disorders. A model outlining this hypothesised relationship is developed throughout the review. It is suggested that eating disorders and anxiety disorders might share common aetiological factors, and that these factors can increase an individual's susceptibility to either disorder. Potential implications for the treatment of eating disorders are outlined, and suggestions are made for further research. It is difficult to establish accurate prevalence rates for eating disorders, both due to variations in methods used for diagnosis and because much of the research has focused exclusively on the diagnoses of anorexia nervosa and bulimia nervosa. Hoek, 1993 and Hoek, 2002 describes how two-stage surveys (using screening measures followed by strict diagnostic interviews) yield lower prevalence rates than earlier surveys based solely on questionnaires. On the basis on these methods, he suggests that the average point prevalence rates amongst females1 are just 0.28% for anorexia nervosa and approximately 1.0% for bulimia nervosa. However, based on a range of epidemiological studies (including Hoek's, 1993 review), Fairburn and Harrison (2003) suggest slightly higher prevalence figures of 0.7% for anorexia nervosa, and 1–2% for bulimia nervosa. Indeed, these rates are relatively consistent with the American Psychiatric Association's prevalence estimates of 0.5–1% for anorexia nervosa, and 1–3% for bulimia nervosa (American Psychiatric Association, 1994). Of course, none of these prevalence figures takes into account the diagnosis of ‘eating disorder not otherwise specified’ (EDNOS; DSM-IV, American Psychiatric Association, 1994), or the equivalent in ICD-10 of ‘atypical eating disorders’ (World Health Organisation, 1992). These disorders appear to be at least as common in clinical practice as anorexia nervosa and bulimia nervosa combined (Fairburn and Harrison, 2003 and Fairburn and Walsh, 2002), and consequently Fairburn and Walsh (2002) suggest that current prevalence rates underestimate the true number of eating disorder cases. Indeed, Grilo (2002) cites evidence that binge eating disorder (one of the EDNOS disorders described in DSM-IV), has prevalence rates of around 2–3% in community samples. Despite the lack of clarity regarding their prevalence, it is clear that an eating disorder can impact negatively on the sufferer's quality of life. Furthermore, eating disorders have been associated with a high rate of psychiatric comorbidity. For example, Braun, Sunday, and Halmi (1994) reported that 81.9% of their sample of women with eating disorders had at least one Axis I comorbidity, with depression, anxiety, and substance misuse being especially common. Moreover, 69% of this sample met criteria for at least one personality disorder. Since the presence of comorbidities is likely to complicate the formulation and treatment of eating disorders (O'Brien & Vincent, 2003), there is a clinical need to understand more about their prevalence. Of particular interest in this review are the different manifestations of anxiety found to be comorbid with eating disorders. Although depression is the most frequently diagnosed comorbid disorder (e.g., Braun et al., 1994 and Herzog et al., 1992), eating disorder patients have reported that anxiety and anger are more likely to drive binges than depression (Arnow, Kenardy, & Agras, 1992). In addition, anxiety has been associated with further disordered eating behaviours, including vomiting (Carter & Duncan, 1984), laxative abuse (Weltzin, Bulik, McConaha, & Kaye, 1995), and restriction (Chesler, 1995). Moreover, Weltzin et al. (1995) suggest that significant anxiety not only reduces compliance with therapy, but also often leads to premature termination of treatment. However, it remains the case that the great majority of the evidence for anxiety as a risk factor in the eating disorders comes from retrospective studies (e.g., Jacobi, Hayward, de Zwann, Kraemer, & Agras, 2004), and that almost all the evidence of causal impact of emotional factors comes from experimental studies that have manipulated depression rather than enxiety (e.g., Stice, 2002). Therefore, the potential for understanding the role of anxiety in the development and maintenance of the eating disorders is still to be realised. In this review of anxiety in the eating disorders, we begin by briefly outlining the general cognitive theory of anxiety. We then discuss the patterns of comorbidity associated with eating disorders and anxiety disorders, and delineate potential temporal relationships between these conditions. We go on to discuss how both safety behaviours and cognitive avoidance strategies might be potential mechanisms linking anxiety and eating pathology, and consider how cognitive avoidance strategies relate to information processing models of anxiety. To conclude the review, we consider both potential implications for the treatment of eating disorders and avenues for future research.

Beck et al. have proposed a cognitive model of anxiety disorders (Beck, Emery, & Greenberg, 1985), which has been adapted and elaborated by numerous authors, including Beck and Clark (1997). According to the Beck et al. (1985) model, the central problem of anxiety involves the allocation of excessive threat meaning to innocuous situations or stimuli, along with an underestimation of personal coping resources. They propose that this bias results in cognitive, affective, physiological, and behavioural changes in the individual (Beck et al., 1985). Cognitive effects might include fear- and vulnerability-related beliefs and images, difficulty concentrating and reasoning, and hypervigilance for threat. These factors are likely to intensify the threat meaning assigned to the object or situation. Physiologically, autonomic hyperarousal occurs in preparation for the fight, flight, freeze, or faint response, and consequently the individual may be behaviourally mobilized (to fight or escape). However, this preparation for action may be experienced as aversive physical symptoms (such as palpitations, breathlessness, or dizziness), which further increase the individual's emotional arousal (e.g., Wells, 1997). An alternative physiological reaction suggested by Beck et al. (1985) is that motor responses may be deactivated, resulting in immobilisation and feelings of helplessness and increased vulnerability. In an attempt to prevent the anxiety response outlined above, anxious individuals inhibit risk-taking and maximise safety-seeking and avoidance. However, as with escape, the use of safety behaviours and avoidance strategies prevent the individual from learning that the imagined threat might be exaggerated (e.g., Wells, 1997). Hence, anxiety is maintained. The above account gives a general description of the cognitive theory of anxiety. However, anxiety is a broad concept incorporating a range of diagnoses, and of course the particular form anxiety takes may be different in different diagnoses. Hence, not all anxiety disorders will be equally associated with eating disorders. The following section will therefore consider the patterns of comorbidity found amongst eating disorders and a range of anxiety disorders. 2. Phenomenological associations between anxiety and the eating disorders In this section, we consider phenomenological patterns of comorbidity between specific anxiety diagnoses and the eating disorders, and the developmental sequencing of those patterns. However, much of the research cited in this review is correlational in nature. It should therefore be remembered that whilst associations between disorders may suggest possible aetiological links, causation cannot be inferred from correlation. In the following section, we consider the causality behind those relationships.