Academic journal article
By Miller, Debra A. F.; McCluskey-Fawcett, Kathleen; Irving, Lori M.
Adolescence , Vol. 28, No. 111
Bulimia nervosa, only formally recognized by the American Psychiatric Association in 1980, is a disorder in which an individual rapidly consumes an unusually large amount of food. This "binge" is terminated by vomiting, laxative abuse, abdominal pain, or sleep, and is seen by the individual as abnormal and distressing (American Psychiatric Association, 1980). This condition is also associated with a strong drive to remain or become thin, as well as a preoccupation, even obsession, with food and eating (Boskind-White & White, 1983).
Reports of the prevalence of this disorder vary widely. In a recent epidemiological report, Fairburn and Beglin (1990) analyzed the incidence data on bulimia nervosa from over 50 publications. They found reports of the prevalence of bulimia in adolescent and young adult women to range from 1% to 35%. Fairburn and Beglin believe that these marked discrepancies are due to a number of factors, including nonstandard diagnostic criteria, self-report data, and sampling procedures. They conclude that bulimia nervosa is probably truly present in only 1% of the population of adolescent and young adult women. Other recent reports, however, suggest that the incidence is between 4% and 8% of young women (Heatherton & Baumeister, 1991). Although these percentages are relatively low, they do represent a large number of young women who are suffering from this serious, sometimes life-threatening psychiatric disorder.
Although bulimia nervosa has received a great deal of attention in the lay press and from clinicians and researchers, there is still remarkably little consensus as to the origins of the disorder. Theories span the continuum of causation from those which are primarily biological (Mitchell & Eckert, 1987) to the heavily sociocultural (Irving, 1990). Markedly absent from many of these theoretical explanations is the developmental history of the individuals with this disorder (Attie & Brooks-Gunn, 1989). For most bulimics, the onset of symptoms does not occur until middle to late adolescence. This late onset has tended to focus investigation of etiology on the adolescent stage rather than on possible earlier childhood precursors. The other issue of possibly critical importance in undercovering the origins of this disorder is why food becomes the focus for these young women as opposed to other types of self-destructive behaviors, such as alcohol abuse or sexual acting out. A brief review of the major theories on the origin of this disorder is useful in examining these issues.
Several reports suggest that there may be a genetic risk for anorexia nervosa, but no such data are yet available on bulimia nervosa (Mitchell & Eckert, 1987). Studies of the basic psychobiological factors involved in bulimia nervosa are equally inconclusive (Mitchell & Eckert, 1987). Treatment studies have, however, demonstrated some limited success in the use of psychotropic drugs, particularly antidepressants, in the alleviation of bulimic symptomatology (Mitchell & Eckert, 1987). Reports of family histories of alcoholism and other addictive behaviors and the presence of depressive and anxiety disorders suggest possible biological origins (Strober & Humphrey, 1987). To date, however, relatively little empirical data support a purely biological basis for bulimia.
The physical changes during adolescence were implicated as a causal variable in eating problems in early adolescence in a two-year longitudinal study by Attie and Brooks-Gunn (1989). The rapid onset of weight gain during the pubertal transition period was suggested as a possible "triggering event" for eating problems, particularly for adolescents with negative body images. The authors postulate that early attempts to control the pubertal weight gain by dieting, coupled with poor physical self-image, may lead to the development of seriously disordered eating patterns in later adolescence.
Cognitive-behavioral models have also been espoused. …