The purpose of this study was to propose and test a model of attachment insecurity in a clinical sample of 268 eating disordered women. Structural relationships among attachment insecurity, BMI, perceived pressure to diet, body dissatisfaction, restrained eating, and negative affect were assessed. A heterogeneous sample of treatment seeking women with a diagnosed eating disorder completed psychometric tests prior to receiving treatment. The data were analysed using structural equation modeling. Fit indices indicated that the hypothesized model fit adequately to the data. Although cross-sectional in nature, the data suggested that attachment insecurity may lead to negative affect. As well, attachment insecurity may lead to body dissatisfaction, which in turn may lead to restrained eating among women with eating disorders. Attachment insecurity could be a possible vulnerability factor for the development of eating disorder symptoms among women.
Researchers have investigated the role of negative affect and dietary restraint as common pathways to bulimic symptoms (e.g., Stice, 2001). Such models indicate that social pressure to be thin and an internalization of a thin ideal body lead to body dissatisfaction. In turn, body dissatisfaction leads to negative affect and dietary restraint, both of which result in bulimic symptoms. Longitudinal data have supported such models (see Stice, 2001 for a review). In a recent study, Duemm, Adams, and Keating (2003) added sociotropy, a measure of interpersonal dependency, to such a model. These authors found a significant relationship between sociotropy and both negative affect and ideal body internalization. Although these structural models have been tested with college women and adolescent girls (Duemm et al., 2003 and Stice et al., 1998), no studies appear to have tested similar models in a clinical sample.
The goal of this study was to assess whether attachment insecurity was related to negative affect and restrained eating in a structural model among women with a diagnosed eating disorder. Attachment insecurity (Bowlby, 1988) (i.e., attachment anxiety and attachment avoidance) was hypothesized to play a role in the development and maintenance of eating disorder symptoms, although the nature of this role remains largely unknown due to a paucity of research (Ward, Ramsey, & Treasure, 2000). In one study in this area, Ward, Ramsey, Turnbull, Benedettini, and Treasure (2000) found that individuals with eating disorders scored higher than a comparison group on measures of attachment anxiety and attachment avoidance, but no differences were found among individuals with different eating disorder diagnoses.
For the current investigation, it was hypothesized that attachment insecurity would influence the development of eating disorder symptoms through negative affect. That is, attachment insecurity influences negative affect which, in turn, influences eating disordered behavior. Research has supported the relationship between negative affect and eating disorder symptoms (e.g., Stice, 2001). Avoidant and anxious attachment styles have been associated with binge eating under stress (Brennan & Shaver, 1995), and binge eating has been conceptualized as a maladaptive means of coping with stress (Wonderlich, Mitchell, Peterson, & Crow, 2001).
Further, attachment avoidance was associated with dietary restraint and a lack of interoceptive awareness, both of which were associated with anorexic symptoms (Brennan & Shaver, 1995).
A second path by which attachment insecurity could lead to eating disorder symptoms (e.g., dietary restraint) is through body dissatisfaction. Duemm et al. (2003) found a relationship between interpersonal dependence and ideal body internalization, which is known to be correlated with body dissatisfaction. Hence, in the current study, it was predicted that attachment insecurity, which encompasses aspects of interpersonal dependence, would be related to body dissatisfaction. A number of other directional relationships (i.e., paths) were hypothesized based on previous research with non-clinical samples (e.g., Duemm et al., 2003 and Stice, 2001). The hypothesized model tested in the present study is presented in Fig. 1.
