Are Eating Disorders Genetic?

Research studies support the genetic influence on eating disorders, but there is not a conclusive agreement on the “candidate genes.”

Research Studies Support Genetic Influence


Formal genetic studies on twins and families have suggested a substantial genetic influence for the three types of eating disorders: anorexia nervosa (AN), bulimia nervosa (BN) and binge eating disorder (BED).


Twin studies show that the heritability rate ranges from 0.48 to 0.74, meaning that up to 74% of phenotypic variation can be explained by additive genetic factors. Heritability of BN is estimated to be between 0.55 and 0.62. As for BED, twin studies have estimated its heritability to be between 0.39 and 0.45.


Eating disorders (ED) are also strongly familial. For example, researchers find that the relative risk for AN is elevated fourfold in family members of AN probands, and female relatives of AN patients are up to eleven times more likely to develop AN than individuals who do not have relatives with AN.


In one family study, 158,697 children with an age range between 12 and 24 years were included and were followed for a median of 5.4 years between 1996 and 2007.


This study found good evidence that ED in parents is associated with ED in their children. The observed association between parental history of ED and ED incidence in children was robust and appeared to be independent of a range of other risk factors. Specifically, rates of eating disorders are twofold higher in the offspring of parents with a diagnosed eating disorder.


Genes That May Cause Eating Disorders


Over the years, many researchers have conducted “candidate-gene” studies to determine the gene(s) that may be responsible for various eating disorders.


Overall, findings suggest that serotonin, brain-derived neurotrophic factor (BDNF), and estrogen genes may be important for the development of the disorders. These neuronal systems influence behavioral and personality characteristics (e.g., anxiety, food intake) that are disrupted in eating disorders.


Serotonin is a neurotransmitter that functions in the brain to control appetite, mood, sleep, memory, and learning. Because of the important role serotonin plays in eating behavior and the documented serotonergic abnormalities in EDs, serotonergic genes and their involvement in EDs have been studied extensively.


BDNF is a protein that acts within the brain to support the growth, differentiation, and survival of new and existing neurons. Increased BDNF causes appetite suppression and weight loss, whereas decreased levels cause weight gain.


Estrogens play a critical role in normal food intake. This gene has been implicated in the organization of neuronal systems involved in eating and activation of patterns of disordered eating.


Because both estrogens and serotonin contribute to general brain arousal, disturbances in either or both systems may contribute to dysregulation in eating behavior by over-preparing the individual to seek and consume food or under-preparing the individual to stop eating.


It should be noted that results from such candidate-gene studies are not conclusive, primarily because candidate-gene findings did not replicate due to small sample sizes, and there are also issues regarding the lack of rigorous correction for multiple testing, methodological heterogeneity, and potential population stratification.

Sources consulted:

Bould, H., et al. “Do eating disorders in parents predict eating disorders in children? Evidence from a Swedish cohort.” Acta Psychiatrica Scandinavica, vol. 132, 2015, pp. 51–59.

Klump, Kelly L. and Kristen M. Culbert. “Molecular Genetic Studies of Eating Disorders Current Status and Future Directions.” Current Directions in Psychological Science, vol. 16, no. 1, 2007, pp. 37-41.

Yilmaz, Zeynep, et al. “Genetics and epigenetics of eating disorders.” Advances in Genomics and Genetics, vol. 5, 2015, pp. 131–150.

Hildebrandt, Tom, et al. “Conceptualizing the role of estrogens and serotonin in the development and maintenance of bulimia nervosa.” Clinical Psychology Review, vol. 30, no. 6, 2010, pp. 655-668.

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