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A ghrelin gene variant may predict crossover rate from restricting-type anorexia nervosa to other phenotypes of eating disorders: a retrospective survival analysis

Ando, Tetsuyaa; Komaki, Gena; Nishimura, Hirokia; Naruo, Tetsurod; Okabe, Kenjiroe; Kawai, Keisukef; Takii, Masatof; Oka, Takakazuf; Kodama, Naokig; Nakamoto, Chiemih; Ishikawa, Toshioi; Suzuki-Hotta, Marib; Minatozaki, Kazunorij; Yamaguchi, Chikaram; Nishizono-Maher, Ayac; Kono, Masakik; Kajiwara, Soheip; Suematsu, Hiroyukin; Tomita, Yuichiroq; Ebana, Shoichiq; Okamoto, Yuril; Nagata, Katsutaror; Nakai, Yoshikatsus; Koide, Masanorio; Kobayashi, Nobuyukit; Kurokawa, Nobuou; Nagata, Toshihikov; Kiriike, Nobuov; Takenaka, Yoshitow; Nagamine, Kiyohidex; Ookuma, Kazuyoshiz; Murata, Shihoy; the Japanese Genetic Research Group for Eating Disorders

doi: 10.1097/YPG.0b013e32833a1f0e
Original Articles

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.

aDepartment of Psychosomatic Research, National Institute of Mental Health, National Center of Neurology and Psychiatry, Kodaira

bHealth Services Center, National Graduate Institute for Policy Studies

cTokyo Institute of Psychiatry, Research for the Promotion of Child and Adolescent Mental Health, Tokyo

dDepartment of Psychosomatic Medicine, Nogami Hospital, Kagoshima

eDepartment of Psychosomatic Medicine, Tenri Hospital, Nara

fDepartment of Psychosomatic Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka

gDivision of Psychosomatic Medicine, Department of Neurology, University of Occupational and Environmental Health, Kitakyushu

hDepartment of Psychosomatic Medicine, Saitama Social Insurance Hospital, Saitama

iDepartment of Body-Mind Medicine, Kohnodai Hospital, International Medical Center of Japan, Ichikawa

jNational Hospital Organization, Hiroshima-nishi Medical Center

kHiroshima Prefectural Nursing, Support Center Wakaba-Ryoikuen Hospital

lHealth Service Center, Hiroshima University, Higashihiroshima, Hiroshima

mDivision of General Medicine, Aichi Medical University Hospital

nSchool of Human Care Studies, Nagoya University of Arts and Sciences

oDepartment of Psychosomatic Medicine, Hoshigaoka Maternity Hospital, Aichi

pNational Sanatorium Io Hospital, Kanazawa

qDepartment of Psychosomatic Medicine, Yokohama Rosai Hospital, Kanagawa

rDepartment of Psychosomatic Medicine, Hamamatsu University Hospital, Shizuoka

sKarasuma Oike Nakai Clinic, Kyoto

tTakano Hospital, Kumamoto

uKurokawa Internal Medicine Clinic (Kurokawa Psychological Laboratory)

vDepartment of Neuropsychiatry, Osaka City University Graduate School of Medicine

wTakenaka Kids Clinic, Osaka

xSuzaka Psychosomatic Medicine Clinic

yAzumi General Hospital, Nagano

zDepartment of Internal Medicine, Yufuin Kosei-nenkin Hospital, Oita, Japan

Correspondence to Tetsuya Ando, MD, PhD, Department of Psychosomatic Research, National Institute of Mental Health, National Center of Neurology and Psychiatry, Ogawahigashicho, Kodaira, Tokyo, Japan

Tel: +42 341 2711; fax: +42 346 1959; e-mail: ando-t@ncnp.go.jp

T.A. participated in the design of the study, conducted the genetic analysis and the statistical analysis, and drafted the manuscript. G.K. conceived the study design, directed the collection of DNA samples and clinical data. H.N. participated in preparing the data set. T.N., K.O., K.K., M.T., N.K., T.O., C.N., T.I., M.S.-H., K.M., C.Y., A.N.-M., M.K., S.K., H.S., Y.T., S.E., Y.O., K.N., Y.N., M.K., N.K., N.K., T.N., N.K., Y.T., K.N., K.O., S.M. and the Japanese Genetic Research Group for Eating Disorders collected the DNA samples and the clinical data.

Received 20 January 2009 Revised 27 August 2009 Accepted 22 November 2009

© 2010 Lippincott Williams & Wilkins, Inc.