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Please use this identifier to cite or link to this item: http://hdl.handle.net/10373/100

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Title: Further evidence of association of OPRD1 & HTR1D polymorphisms with susceptibility to anorexia nervosa
Authors: Brown, Kirsty M.O.
Bujac, Sarah R.
Mann, Evleen T.
Campbell, David A.
Stubbins, Michael J.
Blundell, John E.
Kiezebrink, Kirsty
Affiliation: University of Abertay Dundee. School of Contemporary Sciences
Keywords: Anorexia nervosa
Eating disorders
Serotonin
OPRD1
Issue Date: Feb-2007
Publisher: Elsevier
Type: Journal Article
Refereed: peer-reviewed
Rights: (c) Society of Biological Psychiatry Published by Elsevier Inc. Available from http://dx.doi.org/10.1016/j.biopsych.2006.04.007
Citation: Brown, K.M.O. et al. 2007. Further evidence of association of OPRD1 & HTR1D polymorphisms with susceptibility to anorexia nervosa. Biological Psychiatry 61(3). pp.367-373. http://dx.doi.org/10.1016/j.biopsych.2006.04.007
Abstract: Background: A recent study reported strong evidence for the involvement of a region on human chromosome 1 and genetic susceptibility to anorexia nervosa (AN). A more detailed analysis of this region has suggested 2 genes that may account for this susceptibility. These data suggest that polymorphisms in both the serotonin 1D (HTR1D) and opioid delta 1 (OPRD1) receptor genes show a significant association with restricting AN (RAN). Methods: In the current study, we have conducted an independent association study on 226 females meeting DSM-IV criteria for AN and 678 matched volunteers. Results: We genotyped 4 SNPs in HTR1D and 6 SNPs in OPRD1. 3 SNPs were found to be associated with both RAN and binge-purge AN (BPAN) within the gene for OPRD1. We also found evidence of association between 2 polymorphisms within HTR1D and RAN. Conclusions: These data support the hypothesis that polymorphisms within this region form a component of the genetic basis to susceptibility to RAN. However, further work is required to understand the processes that may be mediated by these genes.
URI: http://hdl.handle.net/10373/100
Appears in Collections:Science Engineering & Technology Collection

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