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: firstname.lastname@example.org
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