In 2000, researchers identified genetic susceptibility for anorexia and bulimia, binge eating disorder and obesity as well as for substance abuse, anxiety, and major depression. Family and twin studies have shown that relatives of someone with an eating disorder are at increased risk for developing a disorder because of a genetic component present in all eating disorders. Studies have shown that 58% – 76% of the incidences of anorexia may be due to genetic factors.
An upcoming issue of the International Journal of Eating Disorders will publish ground-breaking new research by Dr. Howard Steiger that is likely to change our view of anorexia nervosa and its origins. The current project used genetic information from 1,200 anorexia patients and nearly 2,000 non-anorexic controls.
In the new report, researchers found that the longer people suffer from anorexia, the higher the likelihood of alterations in their DNA, specifically in DNA methylation, which can cause changes in an individual’s physiological and emotional make-up.
Dr. Steiger says the study demonstrates a relationship between anorexia and alterations of methylation levels in genes having to do with anxiety, social behavior, various brain functions, and the function of different organs. When gene expression is altered, the expression of traits that are controlled by those genes is also changed. Steiger states that we may come to the conclusion that eating disorders are not just about body image or bad parenting.
“These findings help clarify the point that eating disorders are not about superficial body image concerns or the result of bad parenting,” says Steiger. “They represent real biological effects of environmental impacts in affected people. Here we have physical mechanisms acting upon physiological and nervous system functions throughout the body that may underlie many of the effects of long-term anorexia. The question is, ‘Does remission of AN symptoms coincide with normalization of methylation levels?’”
Every day women are exposed to media of all kinds, movies, TV, magazines and social media that drive home the importance of being thin. But somehow all of these women don’t become anorexic or develop what’s called a “thin-ideal internalization.” Genetic factors may make certain women more susceptible to the pressure to be thin.
In each cell chemical reactions activate and deactivate parts of the genome at strategic times and in specific locations. Epigenetics is the study of these chemical reactions and the factors that influence them. Epigenetics involves genetic control by factors other than an individual’s DNA sequence. DNA methylation is used in some genes to differentiate which gene copy is inherited from the father and which gene copy is inherited from the mother, a phenomenon known as imprinting.
The epigenome dynamically responds to the environment. Stress, diet, behavior, toxins, and other factors regulate gene expression. Many brain functions are accompanied at the cellular level by changes in gene expression. Epigenetic mechanisms such as histone modification and DNA methylation stabilize gene expression, which is important for long-term storage of information.
Not surprisingly, epigenetic changes are also a part of brain diseases such as mental illness and addiction. Understanding the role of epigenetics in brain dysfunction may open the door to being able to influence it. This may lead to the development of new and more effective treatments for brain dysfunctions.
Eating disorders are complex psychiatric disorders in which genes, environment, and gene-environment interactions have a role. The combination of genes and environment can be modified by factors such as malnutrition or stress and this may result in long-term or acute epigenetic modifications.
Genetic variations can contribute to the pathophysiology of eating disorders such as anorexia nervosa or bulimia nervosa. The interplay between genetic and environmental factors is just beginning to be understood. This is the first study reporting alterations of global and gene-specific DNA methylation in a sample of patients with eating disorders.
Steiger’s discovery is important and will lead the way for further research perhaps by learning how to modify epigenetic changes in cells affecting a person’s physiology and nervous system. Will it be possible to prevent more pronounced alterations of methylation levels? When an anorexic patient goes into remission, are changes in methylation levels permanent or will they coincide with recovery? Can we develop medications that will affect methylation levels?
The possibilities for healing the human genome are endless.
References
Freiling, H., Gozner, A., Romer, K., Lenz, B., Bonsch, D., Wilhelm, J., Hillenmacher, T., de Zwaan, M., Kornhuber, J., and Bleich, S. (2007) Global DNA hypomethylation and DNA hypermethylation of the alpha synuclein promoter in females with anorexia nervosa. In Molecular Psychiatry, 12, 229-230.
Frieling, H., Romer, K., Scholz, S., Mittlebach, F., Wilhelm, J., De Zwann, M., Jacoby, G., Kornhuber, J., Hillemacher, T., and Bleich, S. (2009). Epigenetic dysregulation of dopaminergic genes in eating disorders. In International Journal of Eating Disorders, 7, 577-583.
Pjetri, E., et al. (2012). Quantitative promoter DNA methylation analysis of four candidate genes in anorexia nervosa: A pilot study, Journal of Psychiatric Research, http://dx.doi.org.1016/j.jpsychires.2012.10.007.
Pjetri, E., Schmidt, U., Kas, M., and Campbell, I. (2012). Epigenetics and eating disorders. In Current Opinion in Clinical Nutrition and Metabolic Care, 15 (4), 330-335.
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