Complex segregation analysis of obsessive-compulsive disorder in 141 families of eating disorder probands, with and without obsessive-compulsive disorder

Probands affected with eating disorders (ED) present a higher number of rel atives affected with obsessive-compulsive disorders/tic disorders than a co mparison population. Therefore, we hypothesized that ED and obsessive-compu lsive disorder (OCD) might share the same biological liability, and that a single major gene might account for that liability. We tested this hypothes is by applying a complex segregation analysis to 141 families of probands a ffected with ED (89 with anorexia nervosa, restricting and binge-eating typ es, 52 with bulimia nervosa). Given the hypothesized relationship between O CD and genetic spectrum disorders, we considered these diagnoses as affecte d phenotype in relatives. In Italian ED families, ED and OCD followed a Men delian dominant model of transmission. When probands were divided according to co-diagnosis of OCD, best fit in the subgroup of families of 114 proban ds without OCD co-diagnosis was for a Mendelian dominant model of transmiss ion whereas a Mendelian additive model of transmission represented best fit in the subgroup of families of 27 probands with an OCD co-diagnosis. Genet ic transmission was not shown in those families where the only affected phe notype was ED. The existence of a Mendelian mode of genetic transmission wi thin ED families supports the hypothesis that a common genetic liability co uld account for both ED and OCD. Am. J. Med. Genet. (Neuropsychiatr. Genet. ) 96:384-391, 2000, (C) 2000 Wiley-Liss, Inc.