File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Individual-specific risk factors for anorexia nervosa: A pilot study using a discordant sister-pair design

TitleIndividual-specific risk factors for anorexia nervosa: A pilot study using a discordant sister-pair design
Authors
Issue Date2001
PublisherCambridge University Press. The Journal's web site is located at http://journals.cambridge.org/action/displayJournal?jid=PSM
Citation
Psychological Medicine, 2001, v. 31 n. 2, p. 317-329 How to Cite?
AbstractBackground. The aim of this pilot study was to examine which unique factors (genetic and environmental) increase the risk for developing anorexia nervosa by using a case-control design of discordant sister pairs. Methods. Forty-five sister-pairs, one of whom had anorexia nervosa and the other did not, were recruited. Both sisters completed the Oxford Risk Factor Interview for Eating Disorders and measures for eating disorder traits, and sib-pair differences. Blood or cheek cell samples were taken for genetic analysis. Statistical power of the genetic analysis of discordant same-sex siblings was calculated using a specially written program, DISCORD. Results. The sisters with anorexia nervosa differed from their healthy sisters in terms of personal vulnerability traits and exposure to high parental expectations and sexual abuse. Factors within the dieting risk domain did not differ. However, there was evidence of poor feeding in childhood. No difference in the distribution of genotypes or alleles of the DRD4, COMT, the 5HT2A and 5HT2C receptor genes was detected. These results are preliminary because our calculations indicate that there is insufficient power to detect the expected effect on risk with this sample size. Conclusions. A combination of intrinsic and extrinsic factors increases the risk of developing anorexia nervosa. It would, therefore, be informative to undertake a larger study to examine in more detail the unique genetic and environmental factors that are associated with various forms of eating disorders.
Persistent Identifierhttp://hdl.handle.net/10722/175843
ISSN
2021 Impact Factor: 10.592
2020 SCImago Journal Rankings: 2.857
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKarwautz, Aen_US
dc.contributor.authorRabeHesketh, Sen_US
dc.contributor.authorHu, Xen_US
dc.contributor.authorZhao, Jen_US
dc.contributor.authorSham, Pen_US
dc.contributor.authorCollier, DAen_US
dc.contributor.authorTreasure, JLen_US
dc.date.accessioned2012-11-26T09:01:44Z-
dc.date.available2012-11-26T09:01:44Z-
dc.date.issued2001en_US
dc.identifier.citationPsychological Medicine, 2001, v. 31 n. 2, p. 317-329en_US
dc.identifier.issn0033-2917en_US
dc.identifier.urihttp://hdl.handle.net/10722/175843-
dc.description.abstractBackground. The aim of this pilot study was to examine which unique factors (genetic and environmental) increase the risk for developing anorexia nervosa by using a case-control design of discordant sister pairs. Methods. Forty-five sister-pairs, one of whom had anorexia nervosa and the other did not, were recruited. Both sisters completed the Oxford Risk Factor Interview for Eating Disorders and measures for eating disorder traits, and sib-pair differences. Blood or cheek cell samples were taken for genetic analysis. Statistical power of the genetic analysis of discordant same-sex siblings was calculated using a specially written program, DISCORD. Results. The sisters with anorexia nervosa differed from their healthy sisters in terms of personal vulnerability traits and exposure to high parental expectations and sexual abuse. Factors within the dieting risk domain did not differ. However, there was evidence of poor feeding in childhood. No difference in the distribution of genotypes or alleles of the DRD4, COMT, the 5HT2A and 5HT2C receptor genes was detected. These results are preliminary because our calculations indicate that there is insufficient power to detect the expected effect on risk with this sample size. Conclusions. A combination of intrinsic and extrinsic factors increases the risk of developing anorexia nervosa. It would, therefore, be informative to undertake a larger study to examine in more detail the unique genetic and environmental factors that are associated with various forms of eating disorders.en_US
dc.languageengen_US
dc.publisherCambridge University Press. The Journal's web site is located at http://journals.cambridge.org/action/displayJournal?jid=PSMen_US
dc.relation.ispartofPsychological Medicineen_US
dc.subject.meshAdolescenten_US
dc.subject.meshAdulten_US
dc.subject.meshAllelesen_US
dc.subject.meshAnorexia Nervosa - Etiology - Genetics - Psychologyen_US
dc.subject.meshCase-Control Studiesen_US
dc.subject.meshChilden_US
dc.subject.meshFemaleen_US
dc.subject.meshFollow-Up Studiesen_US
dc.subject.meshGenotypeen_US
dc.subject.meshHumansen_US
dc.subject.meshMethyltransferases - Geneticsen_US
dc.subject.meshPilot Projectsen_US
dc.subject.meshQuestionnairesen_US
dc.subject.meshReceptor, Serotonin, 5-Ht2aen_US
dc.subject.meshReceptor, Serotonin, 5-Ht2cen_US
dc.subject.meshReceptors, Dopamine D2 - Geneticsen_US
dc.subject.meshReceptors, Dopamine D4en_US
dc.subject.meshReceptors, Serotonin - Geneticsen_US
dc.titleIndividual-specific risk factors for anorexia nervosa: A pilot study using a discordant sister-pair designen_US
dc.typeArticleen_US
dc.identifier.emailSham, P: pcsham@hku.hken_US
dc.identifier.authoritySham, P=rp00459en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1017/S0033291701003129en_US
dc.identifier.pmid11232918-
dc.identifier.scopuseid_2-s2.0-0035108886en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035108886&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume31en_US
dc.identifier.issue2en_US
dc.identifier.spage317en_US
dc.identifier.epage329en_US
dc.identifier.isiWOS:000167004300012-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridKarwautz, A=7003660154en_US
dc.identifier.scopusauthoridRabeHesketh, S=7003779088en_US
dc.identifier.scopusauthoridHu, X=7404709241en_US
dc.identifier.scopusauthoridZhao, J=7410311266en_US
dc.identifier.scopusauthoridSham, P=34573429300en_US
dc.identifier.scopusauthoridCollier, DA=26642980600en_US
dc.identifier.scopusauthoridTreasure, JL=7006097367en_US
dc.identifier.issnl0033-2917-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats