Biological
Like with anorexia nervosa, there is evidence of genetic predispositions contributing to the onset of this eating disorder. Abnormal levels of many hormones, notablyserotonin, have been shown to be responsible for some disordered eating behaviours. Brain-derived neurotrophic factor (BDNF) is under investigation as a possible mechanism.
There is evidence that sex hormones may influence appetite and eating in women, and the onset of bulimia nervosa. Studies have shown that women with hyperandrogenismand polycystic ovary syndrome have a dysregulation of appetite, along with carbohydrates and fats. This dysregulation of appetite is also seen in women with bulimia nervosa. In addition, gene knockout studies in mice have shown that mice that have the gene encoding estrogen receptors have decreased fertility due to ovarian dysfunction and dysregulation of androgen receptors. In humans, there is evidence that there is an association between polymorphisms in the ERβ (estrogen receptor β) and bulimia, suggesting there is a correlation between sex hormones and bulimia nervosa.
Social
Media portrayals of an 'ideal' body shape are widely considered to be a contributing factor to bulimia. In a 1991 study by Weltzin, Hsu, Pollicle, and Kaye, it was stated that 19% of bulimics undereat, 37% of bulimics eat an amount of food that is normal for an average human being, and 44% of bulimics overeat. A survey of 15–18 year-old high school girls in Nadroga, Fiji found the self-reported incidence of purging rose from 0% in 1995 (a few weeks after the introduction of television in the province) to 11.3% in 1998.
Through the cognitive and socio-cultural perspectives, indications towards the origin of bulimia nervosa can be established. Fairburn et al.’s cognitive behavioral model of bulimia nervosa provides a chief indication of the cause of bulimia through a cognitive perspective, while the “thin ideal” is particularly responsible for the etiology of bulimia nervosa through a socio-cultural context. When attempting to decipher the origin of bulimia nervosa in a cognitive context, Fairburn and et al.’s cognitive behavioral model is often considered the golden standard. Fairburn et al.’s model discusses the process in which an individual falls into the binge-purge cycle and thus develops bulimia. Fairburnet al. argue that extreme concern with weight and shape coupled with low self esteem will result in strict, rigid, and inflexible dietary rules. Accordingly, this would lead to unrealistic restricted eating, which may consequently induce an eventual “slip” where the individual commits a minor infraction of the strict and inflexible dietary rules. Moreover, the cognitive distortion due to dichotomous thinking leads the individual to binge. The binge subsequently should trigger a perceived loss of control, promoting the individual to purge in hope of counteracting the binge. However, Fairburn et al. assert the cycle repeats itself, and thus consider the binge-purge cycle to be self-perpetuating.
In contrast, Byrne and Mclean’s findings differed slightly from Fairburn et al.’s cognitive behavioral model of bulimia nervosa in that the drive for thinness was the major cause of purging as a way of controlling weight. In turn, Byrne and Mclean argued that this makes the individual vulnerable to binging, indicating that it is not a binge-purge cycle but rather a purge-binge cycle in that purging comes before binging. Similarly, Fairburn et al.’s cognitive behavioral model of bulimia nervosa is not necessarily applicable to every individual and is certainly reductionist. Everyone differs from another, and taking such a complex behavior like bulimia and applying the same one theory to everyone would certainly be invalid. In addition, the cognitive behavioral model of bulimia nervosa is very cultural bound in that it may not be necessarily applicable to cultures outside of the Western society. To evaluate, Fairburn et al.’s model and more generally the cognitive explanation of bulimia nervosa is more descriptive than explanatory, as it does not necessarily explain how bulimia arises. Furthermore, it is difficult to ascertain cause and effect, because it may be that distorted eating leads to distorted cognition rather than vice versa.
