|
PMID |
|
|
TITLE |
|
A genome-wide association study of caffeine-related sleep disturbance: confirmation of a role for a common variant in the adenosine receptor. |
|
ABSTRACT |
|
OBJECTIVES |
NlmCategory: OBJECTIVE |
To identify common genetic variants that predispose to caffeine-induced insomnia and to test whether genes whose expression changes in the presence of caffeine are enriched for association with caffeine-induced insomnia. |
DESIGN |
NlmCategory: METHODS |
To identify common genetic variants that predispose to caffeine-induced insomnia and to test whether genes whose expression changes in the presence of caffeine are enriched for association with caffeine-induced insomnia. A hypothesis-free, genome-wide association study. |
SETTING |
NlmCategory: METHODS |
To identify common genetic variants that predispose to caffeine-induced insomnia and to test whether genes whose expression changes in the presence of caffeine are enriched for association with caffeine-induced insomnia. A hypothesis-free, genome-wide association study. Community-based sample of Australian twins from the Australian Twin Registry. |
PARTICIPANTS |
NlmCategory: METHODS |
To identify common genetic variants that predispose to caffeine-induced insomnia and to test whether genes whose expression changes in the presence of caffeine are enriched for association with caffeine-induced insomnia. A hypothesis-free, genome-wide association study. Community-based sample of Australian twins from the Australian Twin Registry. After removal of individuals who said that they do not drink coffee, a total of 2,402 individuals from 1,470 families in the Australian Twin Registry provided both phenotype and genotype information. |
MEASUREMENTS AND RESULTS |
NlmCategory: RESULTS |
To identify common genetic variants that predispose to caffeine-induced insomnia and to test whether genes whose expression changes in the presence of caffeine are enriched for association with caffeine-induced insomnia. A hypothesis-free, genome-wide association study. Community-based sample of Australian twins from the Australian Twin Registry. After removal of individuals who said that they do not drink coffee, a total of 2,402 individuals from 1,470 families in the Australian Twin Registry provided both phenotype and genotype information. A dichotomized scale based on whether participants reported ever or never experiencing caffeine-induced insomnia. A factor score based on responses to a number of questions regarding normal sleep habits was included as a covariate in the analysis. More than 2 million common single nucleotide polymorphisms (SNPs) were tested for association with caffeine-induced insomnia. No SNPs reached the genome-wide significance threshold. In the analysis that did not include the insomnia factor score as a covariate, the most significant SNP identified was an intronic SNP in the PRIMA1 gene (P = 1.4 × 10⁻⁶, odds ratio = 0.68 [0.53 - 0.89]). An intergenic SNP near the GBP4 gene on chromosome 1 was the most significant upon inclusion of the insomnia factor score into the model (P = 1.9 × 10⁻⁶, odds ratio = 0.70 [0.62 - 0.78]). A previously identified association with a polymorphism in the ADORA2A gene was replicated. |
CONCLUSIONS |
NlmCategory: CONCLUSIONS |
To identify common genetic variants that predispose to caffeine-induced insomnia and to test whether genes whose expression changes in the presence of caffeine are enriched for association with caffeine-induced insomnia. A hypothesis-free, genome-wide association study. Community-based sample of Australian twins from the Australian Twin Registry. After removal of individuals who said that they do not drink coffee, a total of 2,402 individuals from 1,470 families in the Australian Twin Registry provided both phenotype and genotype information. A dichotomized scale based on whether participants reported ever or never experiencing caffeine-induced insomnia. A factor score based on responses to a number of questions regarding normal sleep habits was included as a covariate in the analysis. More than 2 million common single nucleotide polymorphisms (SNPs) were tested for association with caffeine-induced insomnia. No SNPs reached the genome-wide significance threshold. In the analysis that did not include the insomnia factor score as a covariate, the most significant SNP identified was an intronic SNP in the PRIMA1 gene (P = 1.4 × 10⁻⁶, odds ratio = 0.68 [0.53 - 0.89]). An intergenic SNP near the GBP4 gene on chromosome 1 was the most significant upon inclusion of the insomnia factor score into the model (P = 1.9 × 10⁻⁶, odds ratio = 0.70 [0.62 - 0.78]). A previously identified association with a polymorphism in the ADORA2A gene was replicated. Several genes have been identified in the study as potentially influencing caffeine-induced insomnia. They will require replication in another sample. The results may have implications for understanding the biologic mechanisms underlying insomnia. |
|
DATE PUBLISHED |
|
|
HISTORY |
|
PUBSTATUS |
PUBSTATUSDATE |
entrez |
2012/07/04 06:00 |
pubmed |
2012/07/04 06:00 |
medline |
2012/11/14 06:00 |
|
AUTHORS |
|
NAME |
COLLECTIVENAME |
LASTNAME |
FORENAME |
INITIALS |
AFFILIATION |
AFFILIATIONINFO |
Byrne EM |
|
Byrne |
Enda M |
EM |
|
Queensland Institute of Medical Research, Brisbane, Australia. enda.byrne@qimr.edu.au |
Johnson J |
|
Johnson |
Julie |
J |
|
|
McRae AF |
|
McRae |
Allan F |
AF |
|
|
Nyholt DR |
|
Nyholt |
Dale R |
DR |
|
|
Medland SE |
|
Medland |
Sarah E |
SE |
|
|
Gehrman PR |
|
Gehrman |
Philip R |
PR |
|
|
Heath AC |
|
Heath |
Andrew C |
AC |
|
|
Madden PA |
|
Madden |
Pamela A F |
PA |
|
|
Montgomery GW |
|
Montgomery |
Grant W |
GW |
|
|
Chenevix-Trench G |
|
Chenevix-Trench |
Georgia |
G |
|
|
Martin NG |
|
Martin |
Nicholas G |
NG |
|
|
|
INVESTIGATORS |
|
|
JOURNAL |
|
VOLUME: 35 |
ISSUE: 7 |
TITLE: Sleep |
ISOABBREVIATION: Sleep |
YEAR: 2012 |
MONTH: Jul |
DAY: 01 |
MEDLINEDATE: |
SEASON: |
CITEDMEDIUM: Internet |
ISSN: 1550-9109 |
ISSNTYPE: Electronic |
|
MEDLINE JOURNAL |
|
MEDLINETA: Sleep |
COUNTRY: United States |
ISSNLINKING: 0161-8105 |
NLMUNIQUEID: 7809084 |
|
PUBLICATION TYPE |
|
PUBLICATIONTYPE TEXT |
Journal Article |
Research Support, N.I.H., Extramural |
Research Support, Non-U.S. Gov't |
Twin Study |
|
COMMENTS AND CORRECTIONS |
|
REFTYPE |
REFSOURCE |
REFPMID |
NOTE |
CommentIn |
Sleep. 2012 Jul;35(7):899-900 |
22754033 |
|
|
GRANTS |
|
GRANTID |
AGENCY |
COUNTRY |
R01 AA007535 |
NIAAA NIH HHS |
United States |
R01 AA014041 |
NIAAA NIH HHS |
United States |
K05 AA017688 |
NIAAA NIH HHS |
United States |
R01 MH066206 |
NIMH NIH HHS |
United States |
AA13320 |
NIAAA NIH HHS |
United States |
AA13321 |
NIAAA NIH HHS |
United States |
AA10248 |
NIAAA NIH HHS |
United States |
R01 AA013326 |
NIAAA NIH HHS |
United States |
MH66206 |
NIMH NIH HHS |
United States |
R01 AA013321 |
NIAAA NIH HHS |
United States |
AA14041 |
NIAAA NIH HHS |
United States |
AA13326 |
NIAAA NIH HHS |
United States |
R01 AA013320 |
NIAAA NIH HHS |
United States |
|
GENERAL NOTE |
|
|
KEYWORDS |
|
KEYWORD |
Caffeine |
genetics |
insomnia |
|
MESH HEADINGS |
|
DESCRIPTORNAME |
QUALIFIERNAME |
Adult |
|
Caffeine |
adverse effects |
Female |
adverse effects |
Gene Expression Profiling |
adverse effects |
Genome-Wide Association Study |
adverse effects |
Genotype |
adverse effects |
Humans |
adverse effects |
Male |
adverse effects |
Membrane Proteins |
physiology |
Nerve Tissue Proteins |
physiology |
Polymorphism, Single Nucleotide |
genetics |
Receptor, Adenosine A2A |
physiology |
Sleep Wake Disorders |
genetics |
|
SUPPLEMENTARY MESH |
|
|
GENE SYMBOLS |
|
|
CHEMICALS |
|
REGISTRYNUMBER |
NAMEOFSUBSTANCE |
0 |
Membrane Proteins |
0 |
Nerve Tissue Proteins |
0 |
PRIMA1 protein, human |
0 |
Receptor, Adenosine A2A |
3G6A5W338E |
Caffeine |
|
OTHER ID's |
|
|
|