Anorexia nervosa (AN) is a potentially chronic illness with extremely high morbidity and mortality for which no generally agreed upon model of etiology presently exists [Sullivan, 1995; Birmingham et al., 2005]. In spite of the chronicity and high economic burden it confers, the effects of currently applied treatment approaches remain largely disappointing. Although psychosocial factors were long implicated in its etiology [Striegel-Moore and Bulik, 2007], a growing body of evidence now supports the role of genetic influences, although no specific variants have been definitively implicated as causal to date [Bulik et al., 2007]. In this light, however, the familiality of AN has now been well established, with first-degree female relatives of individuals with AN having an approximately 10-fold greater lifetime risk of having an eating disorder compared with relatives of unaffected individuals [Lilenfeld et al., 1998; Strober et al., 2000]. Heritability estimates for AN have ranged from 46% to 78% [Wade et al., 2000; Klump et al., 2001; Kortegaard et al., 2001; Bulik et al., 2006]. The convergent findings from family and twin studies have motivated efforts to identify loci that contribute to risk for AN through linkage and association studies.
