ABSTRACT
The current literature on eating disorders is replete with theoretical explanations for the causes of anorexia nervosa (AN) and bulimia nervosa (BN) and with recommendations for the treatment of these disorders (e.g., Alexander & Lumsden, 1994; Brownell & Foreyt, 1986; Bruch, 1973; Crowther, Tennenbaum, Hobfoll, & Stephens, 1992; Johnson, 1991; Johnson & Connors, 1987; Root, Fallon, & Friedrich, 1986). The approaches to understanding eating disorders range from psychodynamic (Bruch, 1973, 1985; Goodsitt, 1985) to cognitive-behavioral (Fairburn, 1985; Garner, 1986) to a consideration offamily systems (Minuchin, Rosman, & Baker, 1978; Sargent, Liebman, & Silver, 1985). Within each of these theoretical orientations, inferences have been made with regard to the primary etiology of the disorder, and an assumption has been made that there is a direct association between predisposing factors and the onset of illness (see, e.g., Becker, Bell, & Billington, 1987; Friedlander & Siegel, 1990). Where the effects of multiple etiological variables have been considered simultaneously (Garfinkel & Garner, 1982; Johnson & Connors, 1987), there is still an implicit assumption that when an eating disorder occurs, these determinants necessarily predispose to illness; what is neglected is a consideration of the actual paths and processes by which, in certain individuals, these diverse factors are transformed over time into disorder.
