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Association study of 182 candidate genes in anorexia nervosa
Author(s) -
Pinheiro Andrea Poyastro,
Bulik Cynthia M.,
Thornton Laura M.,
Sullivan Patrick F.,
Root Tammy L.,
Bloss Cinnamon S.,
Berrettini Wade H.,
Schork Nicholas J.,
Kaye Walter H.,
Bergen Andrew W.,
Magistretti Pierre,
Brandt Harry,
Crawford Steve,
Crow Scott,
Fichter Manfred M.,
Goldman David,
Halmi Katherine A.,
Johnson Craig,
Kaplan Allan S.,
Keel Pamela K.,
Klump Kelly L.,
La Via Maria,
Mitchell James E.,
Strober Michael,
Rotondo Alessandro,
Treasure Janet,
Woodside D. Blake
Publication year - 2010
Publication title -
american journal of medical genetics part b: neuropsychiatric genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.393
H-Index - 126
eISSN - 1552-485X
pISSN - 1552-4841
DOI - 10.1002/ajmg.b.31082
Subject(s) - candidate gene , single nucleotide polymorphism , snp , genetic association , genome wide association study , anorexia nervosa , genetics , haplotype , bulimia nervosa , biology , linkage disequilibrium , eating disorders , gene , psychology , genotype , clinical psychology
We performed association studies with 5,151 SNPs that were judged as likely candidate genetic variations conferring susceptibility to anorexia nervosa (AN) based on location under reported linkage peaks, previous results in the literature (182 candidate genes), brain expression, biological plausibility, and estrogen responsivity. We employed a case–control design that tested each SNP individually as well as haplotypes derived from these SNPs in 1,085 case individuals with AN diagnoses and 677 control individuals. We also performed separate association analyses using three increasingly restrictive case definitions for AN: all individuals with any subtype of AN (All AN: n = 1,085); individuals with AN with no binge eating behavior (AN with No Binge Eating: n = 687); and individuals with the restricting subtype of AN (Restricting AN: n = 421). After accounting for multiple comparisons, there were no statistically significant associations for any individual SNP or haplotype block with any definition of illness. These results underscore the importance of large samples to yield appropriate power to detect genotypic differences in individuals with AN and also motivate complementary approaches involving Genome‐Wide Association (GWA) studies, Copy Number Variation (CNV) analyses, sequencing‐based rare variant discovery assays, and pathway‐based analysis in order to make up for deficiencies in traditional candidate gene approaches to AN. © 2010 Wiley‐Liss, Inc.