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Introduction
To combat any disease, one has to know its etiology that is, the set of causes that lead to the emergence of a medical condition which often proves to be a difficult task. This is precisely the case with anorexia nervosa, one of the most widely spread eating disorders in the Western world. Anorexia causes distorted self-image, a pathological fear of overeating, and an obsessive desire to stay thin up to the point of starvation and usually develops in young women from 15 to 19 (Burkert, 2016).
While some may discard anorexia as merely an unhealthy dietary habit, this is not the case, as it has one of the highest mortality rates among all psychiatric disorders (Le Grange et al., 2016). Ever since the discovery of the disease, researchers have offered numerous explanations focusing on biological and social factors that presumably lead to the condition, and this paper will list these explanations and criticisms against them. Most of the proposed etiologies have been proven wrong, either partially or entirely, but recent studies suggest that genetic predisposition is likely the major cause of anorexia.
Historical Discourse on the Causes of Anorexia
As mentioned above, there is no consensus on the precise etiology of the disorder, as medical professionals have proposed different explanations throughout history. In the second half of the 19th century, Gull and Lasegue, who had first described this disease as a distinctive medical condition, interpreted it as a form of hysteria (Simonovic et al., 2015). In the early 20th century, Simmonds offered another explanation by attributing anorexia to the dysfunction of the pituitary gland (Simonovic et al., 2015).
The psychoanalytical approach of the middle century explained anorexia through underdeveloped sexuality and magical beliefs of becoming pregnant through eating (Simonovic et al., 2015, p. 35). Other approaches arose in the 1960s and stressed the role of family and sociocultural expectations. According to these, anorexia develops because of the societal pressure on a woman to look according to the established beauty standards retranslated through society at large and family in particular (Simonovic et al., 2015). Thus, most etiologies of anorexia developed so far offer a wide range of explanations from psychological to biological, but all these have been subjects to severe criticism.
Criticisms of Historical Etiologies
None of the etiologies of anorexia offered throughout the decades evaded criticism, and most have been proved partially or entirely wrong. The explanation developed by Gull and Lasegue suggested isolating the patient from the family to cure supposed hysteria but, as Le Grange et al. (2016) show, families play a positive role in anorexics recovery. Thus, the original etiology finds no support in clinical practice. The glandular approach was disproven by the 1940s by the experiments demonstrating that pituitary insufficiency had no direct correlation with anorexia (Simonovic et al., 2015).
The psychoanalytical approach rests on a Freudian interpretation of food as an impregnating agent that finds little empirical support (Simonovic et al., 2015). As for the sociocultural explanations that link anorexia to the beauty standards accepted in society, research shows mixed findings concerning a possible association between dieting and the pressure to be thin (Burkert, 2015, p. 36). As one can see, each of the explanations offered up until the 1980s proved to be at least partially wrong.
Genetic Predisposition as an Explanation
After the failure of the glandular approach, researchers avoided focusing on the possible biological causes of anorexia for a long time, but the situation changed in the late 1980s. In a groundbreaking study published in 1988, a group of scientists demonstrated that twins were often concordant for anorexia (Simonovic et al., 2015). Moreover, as much as 5 percent of their first-degree relatives also had a history of anorexia (Simonovic et al., 2015).
These results allowed the authors to conclude that the development of anorexia was to a great extent genetically determined (Simonovic et al., 2015, p. 36). An article by Simonovic et al. (2015) shows that, since its emergence in the late 1980s, the new etiology has displaced the previous ones in the research literature. The fact that, despite such prominence, it had not been disproven in the three following decades suggests that genetic predisposition is likely the foremost cause of anorexia.
Conclusion
As one can see, genetic predisposition currently seems the most plausible explanation among all the proposed etiologies of anorexia. Ever since medical professionals discovered the disease in the 19th century, they offered various explanations for its emergence and development, most of which have been proven wrong by now. The original interpretation of anorexia as hysteria proved to be incompatible with the clinical practice, the glandular approach was refuted experimentally, psychoanalytical interpretation found little evidence in its favor, and sociocultural explanations yielded mixed findings.
On the other hand, the studies of the late 1980s confirmed a strong concordance for anorexia in twins as well as the likelihood for an anorexic to have a family history of the disease. Considering these findings and the fact that they were not disproven in thirty years of research after their announcement, one may assume that genetic predisposition is likely a major cause behind the development of anorexia.
References
Burkert, N. T. (2015). Psychological and Neurobiological Aspects of Eating Disorders: A Taste-fMRI Study in Patients Suffering from Anorexia Nervosa. Springer.
Le Grange, D., Hughes, E. K., Court, A., Yeo, M., Crosby, R. D., & Sawyer, S. M. (2016). Randomized clinical trial of parent-focused treatment and family-based treatment for adolescent anorexia nervosa. Journal of the American Academy of Child and Adolescent Psychiatry, 55(8), 683-692.
Simonovic, S., Cross, D., & Ernst, J. P. (2015). The historical discourse on the etiology of anorexia nervosa: Results of a literature analysis. Sudhoffs Archiv, 99(1), 31-43.
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