TY - JOUR
T1 - A ghrelin gene variant may predict crossover rate from restricting-type anorexia nervosa to other phenotypes of eating disorders
T2 - A retrospective survival analysis
AU - Ando, Tetsuya
AU - Komaki, Gen
AU - Nishimura, Hiroki
AU - Naruo, Tetsuro
AU - Okabe, Kenjiro
AU - Kawai, Keisuke
AU - Takii, Masato
AU - Oka, Takakazu
AU - Kodama, Naoki
AU - Nakamoto, Chiemi
AU - Ishikawa, Toshio
AU - Suzuki-Hotta, Mari
AU - Minatozaki, Kazunori
AU - Yamaguchi, Chikara
AU - Nishizono-Maher, Aya
AU - Kono, Masaki
AU - Kajiwara, Sohei
AU - Suematsu, Hiroyuki
AU - Tomita, Yuichiro
AU - Ebana, Shoichi
AU - Okamoto, Yuri
AU - Nagata, Katsutaro
AU - Nakai, Yoshikatsu
AU - Koide, Masanori
AU - Kobayashi, Nobuyuki
AU - Kurokawa, Nobuo
AU - Nagata, Toshihiko
AU - Kiriike, Nobuo
AU - Takenaka, Yoshito
AU - Nagamine, Kiyohide
AU - Ookuma, Kazuyoshi
AU - Murata, Shiho
PY - 2010/8
Y1 - 2010/8
N2 - Background: Patients with anorexia nervosa restricting type (AN-R) often develop bulimic symptoms and crossover to AN-binge eating/purging type (AN-BP), or to bulimia nervosa (BN). We have reported earlier that genetic variants of an orexigenic peptide ghrelin are associated with BN. Here, the relationship between a ghrelin gene variant and the rate of change from AN-R to other phenotypes of eating disorders (EDs) was investigated. MethodS: Participants were 165 patients with ED, initially diagnosed as AN-R. The dates of their AN-R onset and changes in diagnosis to other subtypes of ED were investigated retrospectively. Ghrelin gene 3056 T→C SNP (single nucleotide polymorphism) was genotyped. Probability and hazard ratios were analyzed using life table analysis and Cox's proportional hazard regression model, in which the starting point was the time of AN-R onset and the outcome events were the time of (i) onset of binge eating, that is, when patients changed to binge eating AN and BN and (ii) recovery of normal weight, that is, when patients changed to BN or remission. Results: Patients with the TT genotype at 3056 T→C had a higher probability and hazard ratio for recovery of normal weight. The ghrelin SNP was not related with the onset of binge eating. Conclusion: The 3056 T→C SNP of the ghrelin gene is related to the probability and the rate of recovery of normal body weight from restricting-type AN.
AB - Background: Patients with anorexia nervosa restricting type (AN-R) often develop bulimic symptoms and crossover to AN-binge eating/purging type (AN-BP), or to bulimia nervosa (BN). We have reported earlier that genetic variants of an orexigenic peptide ghrelin are associated with BN. Here, the relationship between a ghrelin gene variant and the rate of change from AN-R to other phenotypes of eating disorders (EDs) was investigated. MethodS: Participants were 165 patients with ED, initially diagnosed as AN-R. The dates of their AN-R onset and changes in diagnosis to other subtypes of ED were investigated retrospectively. Ghrelin gene 3056 T→C SNP (single nucleotide polymorphism) was genotyped. Probability and hazard ratios were analyzed using life table analysis and Cox's proportional hazard regression model, in which the starting point was the time of AN-R onset and the outcome events were the time of (i) onset of binge eating, that is, when patients changed to binge eating AN and BN and (ii) recovery of normal weight, that is, when patients changed to BN or remission. Results: Patients with the TT genotype at 3056 T→C had a higher probability and hazard ratio for recovery of normal weight. The ghrelin SNP was not related with the onset of binge eating. Conclusion: The 3056 T→C SNP of the ghrelin gene is related to the probability and the rate of recovery of normal body weight from restricting-type AN.
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U2 - 10.1097/YPG.0b013e32833a1f0e
DO - 10.1097/YPG.0b013e32833a1f0e
M3 - Article
C2 - 20421852
AN - SCOPUS:77954887284
SN - 0955-8829
VL - 20
SP - 153
EP - 159
JO - Psychiatric Genetics
JF - Psychiatric Genetics
IS - 4
ER -