Further evidence of association of OPRD1 & HTR1D polymorphisms with susceptibility to anorexia nervosa

Kirsty M.O. Brown; Sarah R. Bujac; Evleen T. Mann; David A. Campbell; Michael J. Stubbins; John E. Blundell; Kirsty Kiezebrink

doi:10.1016/j.biopsych.2006.04.007

Further evidence of association of OPRD1 & HTR1D polymorphisms with susceptibility to anorexia nervosa

Kirsty M.O. Brown, Sarah R. Bujac, Evleen T. Mann, David A. Campbell, Michael J. Stubbins, John E. Blundell, Kirsty Kiezebrink

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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.

Original language	English
Pages (from-to)	367-373
Number of pages	7
Journal	Biological Psychiatry
Volume	61
Issue number	3
DOIs	https://doi.org/10.1016/j.biopsych.2006.04.007
Publication status	Published - Feb 2007
Externally published	Yes

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Brown, K. M. O., Bujac, S. R., Mann, E. T., Campbell, D. A., Stubbins, M. J., Blundell, J. E., & Kiezebrink, K. (2007). Further evidence of association of OPRD1 & HTR1D polymorphisms with susceptibility to anorexia nervosa. Biological Psychiatry, 61(3), 367-373. https://doi.org/10.1016/j.biopsych.2006.04.007

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title = "Further evidence of association of OPRD1 & HTR1D polymorphisms with susceptibility to anorexia nervosa",

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.",

author = "Brown, {Kirsty M.O.} and Bujac, {Sarah R.} and Mann, {Evleen T.} and Campbell, {David A.} and Stubbins, {Michael J.} and Blundell, {John E.} and Kirsty Kiezebrink",

year = "2007",

month = "2",

doi = "10.1016/j.biopsych.2006.04.007",

language = "English",

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pages = "367--373",

journal = "Biological Psychiatry",

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T1 - Further evidence of association of OPRD1 & HTR1D polymorphisms with susceptibility to anorexia nervosa

AU - Brown, Kirsty M.O.

AU - Bujac, Sarah R.

AU - Mann, Evleen T.

AU - Campbell, David A.

AU - Stubbins, Michael J.

AU - Blundell, John E.

AU - Kiezebrink, Kirsty

PY - 2007/2

Y1 - 2007/2

N2 - 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.

AB - 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.

U2 - 10.1016/j.biopsych.2006.04.007

DO - 10.1016/j.biopsych.2006.04.007

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VL - 61

SP - 367

EP - 373

JO - Biological Psychiatry

JF - Biological Psychiatry

IS - 3

ER -

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10.1016/j.biopsych.2006.04.007