Overestimates of the Genetic Contribution to Eating Disorders

2006 ◽  
Vol 8 (2) ◽  
pp. 123-131 ◽  
Author(s):  
Colin A. Ross

The purpose of this article is to analyze and critique repeated claims in the literature that there is a substantial genetic contribution to eating disorders. Data from the existing twin and family studies of eating disorders were tabulated and compared to heritability estimates resulting from complex statistical analyses of the same data. Overall, concordance in monozygotic twins is 26% for bulimia and 35% for anorexia nervosa. Among the relatives of probands with bulimia, 95.1% do not have bulimia, whereas among the relatives of probands with anorexia nervosa, 97.1% do not have the disorder. The raw data refute claims that the genetic heritability of eating disorders is as high as 80%. The erroneous conclusion that there is a substantial genetic contribution to eating disorders needs to be corrected by focusing on the raw data for twin concordance and prevalence in first-degree relatives.

2001 ◽  
Vol 29 (3) ◽  
pp. 263-269 ◽  
Author(s):  
Michael Strober ◽  
Roberta Freeman ◽  
Carlyn Lampert ◽  
Jane Diamond ◽  
Walter Kaye

2018 ◽  
Vol 20 (2) ◽  
pp. 73-78
Author(s):  
Colin A. Ross

The incorrect belief that anorexia nervosa is predominantly genetic is maintained in the psychiatric literature by a series of misquotations and misrepresentations of research data. An example of this type of scholarship is as an editorial in The American Journal of Psychiatry. Data from family and twin studies referenced in the editorial provide compelling evidence that the genetic contribution to the etiology of anorexia nervosa is small. The incorrect belief that anorexia nervosa is predominantly genetic is maintained, in addition, by statistical procedures such as heritability estimates. The incorrect belief that anorexia nervosa is predominantly genetic should not be endorsed by the American Psychiatric Association, in either its journals, in its published books, or in DSM–V.


Author(s):  
R. Mark Beattie ◽  
Anil Dhawan ◽  
John W.L. Puntis

Anorexia nervosa 110Bulimia nervosa 112Eating disorders are defined as persistent disturbance of eating (± behaviour) that impairs physical health or psychosocial functioning or both and that is not secondary to any other medical or psychiatric disorder.Anorexia nervosa is a complex disorder described in a number of different ways and recognized for >100 years. It involves voluntary self-starvation, with weight loss, or avoidance of weight gain during adolescence. Peak age of onset is in mid-teens, with a female to male ratio of 10:1, and a prevalence of around 1%. Genetic factors are important, with 55% of monozygotic twins being concordant for anorexia. Sociocultural factors are highly relevant, with the illness occurring predominantly in Western societies where thinness has become increasingly valued as an element of the feminine ideal. Reported mortality rates vary from 0 to 22%....


2001 ◽  
Vol 31 (2) ◽  
pp. 361-365 ◽  
Author(s):  
L. S. KORTEGAARD ◽  
K. HOERDER ◽  
J. JOERGENSEN ◽  
C. GILLBERG ◽  
K. O. KYVIK

Background. Twin studies have concluded that there is a substantial genetic contribution to the aetiology of eating disorders. The aim of the present study was to estimate the genetic contribution to the aetiology of self-reported eating disorders in a sample of representative twins.Method. A population cohort of 34142 young Danish twins was screened for eating disorders by a mailed questionnaire.Results. Concordance rates differed significantly across monozygotic and dizygotic twin pairs for broadly defined self-reported anorexia nervosa and bulimia nervosa. Heritability estimates of 0·48, 0·52 and 0·61 respectively were estimated for narrow and broad definitions of self-reported anorexia nervosa and for self-reported bulimia nervosa.Conclusions. There is a genetic contribution to the aetiology of self-reported eating disorders in the general population. The relationship between self-reported and clinical eating disorder remains to be examined.


Author(s):  
Susan McElroy ◽  
Anna I. Guerdjikova ◽  
Nicole Mori ◽  
Paul E. Keck

This chapter addresses the pharmacotherapy of the eating disorders (EDs). Many persons with EDs receive pharmacotherapy, but pharmacotherapy research for EDs has lagged behind that for other major mental disorders. This chapter first provides a brief rationale for using medications in the treatment of EDs. It then reviews the data supporting the effectiveness of specific medications or medication classes in treating patients with anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder (BED), and other potentially important EDs, such as night eating syndrome (NES). It concludes by summarizing these data and suggesting future areas for research in the pharmacotherapy of EDs.


Author(s):  
Pamela Keel

The epidemiology of eating disorders holds important clues for understanding factors that may contribute to their etiology. In addition, epidemiological findings speak to the public health significance of these deleterious syndromes. Information on course and outcome are important for clinicians to understand the prognosis associated with different disorders of eating and for treatment planning. This chapter reviews information on the epidemiology and course of anorexia nervosa, bulimia nervosa, and two forms of eating disorder not otherwise specified, binge eating disorder and purging disorder.


Author(s):  
Susan L. McElroy ◽  
Anna I. Guerdjikova ◽  
Anne M. O’Melia ◽  
Nicole Mori ◽  
Paul E. Keck

Many persons with eating disorders (EDs) receive pharmacotherapy, but pharmacotherapy research for EDs has lagged behind that for other major mental disorders. In this chapter, we first provide a brief rationale for using medications in the treatment of EDs. We then review the data supporting the effectiveness of specific medications or medication classes in treating patients with anorexia nervosa (AN), bulimia nervosa, binge eating disorder (BED), and other potentially important EDs, such as night eating syndrome (NES) and sleep-related eating disorder (SRED). We conclude by summarizing these data and suggesting future areas for research in the pharmacotherapy of EDs.


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