Eating Disorders and Obesity: A Comprehensive Handbook

By Christopher G. Fairburn; Kelly D. Brownell | Go to book overview

43
Molecular Genetics
of Eating Disorders

DAVID A. COLLIER

As discussed in Chapter 42, the findings from twin studies suggest that about half the vulnerability to develop eating disorders is inherited. This points to the possibility of finding variation in genes that alters susceptibility to eating disorders—the subject of this chapter.


CONCEPTUAL ISSUES

Unlike Mendelian genetic disorders such as Huntington’s disease, which are caused by the effect of a single gene in each person, “complex” diseases are caused by the interaction of multiple genes with the environment. Thus, for example, a major unfavorable life event might have a much greater effect on somebody who carries a genetic vulnerability to depression than someone who does not. This genetic vulnerability is likely to take the form of many genes of small effect that might increase risk two- or three-fold. These genes will be neither necessary nor sufficient to cause disease (i.e., many, if not most, people who carry them will not become ill). An accumulation of these genes, together with adverse environmental factors, increases risk until the disease develops in those carrying the greatest genetic and environmental loading. This is known as the liability–threshold model.

Although you cannot change your genes any more than you can reverse the event of childhood abuse, complex disease genetics is not deterministic genetics. Risk factors for complex genetic disorders cannot be reliably used to predict who will become ill. Instead, the usefulness of vulnerability genes is in the guidance they provide to the understanding of pathophysiology, which in turn must be helpful in designing new treatments. Finding genes does not mean that psychological treatments will be superseded or neglected; they are an important method of treatment and will remain so.

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