Genotype-covariate interaction effects and the heritability of adult body mass index

Robinson, Matthew R., English, Geoffrey, Moser, Gerhard, Lloyd-Jones, Luke R., Triplett, Marcus A., Zhu, Zhihong, Nolte, Ilja M., Van Vliet-Ostaptchouk, Jana V., Snieder, Harold, Esko, Tonu, Milani, Lili, Magi, Reedik, Metspalu, Andres, Magnusson, Patrik K. E., Pedersen, Nancy L., Ingelsson, Erik, Johannesson, Magnus, Yang, Jian, Cesarini, David and Visscher, Peter M. (2017) Genotype-covariate interaction effects and the heritability of adult body mass index. Nature Genetics, 49 8: 1174-1181. doi:10.1038/ng.3912


Author Robinson, Matthew R.
English, Geoffrey
Moser, Gerhard
Lloyd-Jones, Luke R.
Triplett, Marcus A.
Zhu, Zhihong
Nolte, Ilja M.
Van Vliet-Ostaptchouk, Jana V.
Snieder, Harold
Esko, Tonu
Milani, Lili
Magi, Reedik
Metspalu, Andres
Magnusson, Patrik K. E.
Pedersen, Nancy L.
Ingelsson, Erik
Johannesson, Magnus
Yang, Jian
Cesarini, David
Visscher, Peter M.
Title Genotype-covariate interaction effects and the heritability of adult body mass index
Journal name Nature Genetics   Check publisher's open access policy
ISSN 1546-1718
1061-4036
Publication date 2017-08-01
Year available 2017
Sub-type Article (original research)
DOI 10.1038/ng.3912
Open Access Status Not yet assessed
Volume 49
Issue 8
Start page 1174
End page 1181
Total pages 8
Place of publication New York, NY, United States
Publisher Nature Publishing Group
Language eng
Abstract Obesity is a worldwide epidemic, with major health and economic costs. Here we estimate heritability for body mass index (BMI) in 172,000 sibling pairs and 150,832 unrelated individuals and explore the contribution of genotype-covariate interaction effects at common SNP loci. We find evidence for genotype-age interaction (likelihood ratio test (LRT) = 73.58, degrees of freedom (df) = 1, P = 4.83 × 10(-18)), which contributed 8.1% (1.4% s.e.) to BMI variation. Across eight self-reported lifestyle factors, including diet and exercise, we find genotype-environment interaction only for smoking behavior (LRT = 19.70, P = 5.03 × 10(-5) and LRT = 30.80, P = 1.42 × 10(-8)), which contributed 4.0% (0.8% s.e.) to BMI variation. Bayesian association analysis suggests that BMI is highly polygenic, with 75% of the SNP heritability attributable to loci that each explain <0.01% of the phenotypic variance. Our findings imply that substantially larger sample sizes across ages and lifestyles are required to understand the full genetic architecture of BMI.
Keyword Genetics & Heredity
Genetics & Heredity
Q-Index Code C1
Q-Index Status Provisional Code
Grant ID 12505
160103860
1080157
R21ESO25052-01
421-2013-1061
E9/11
P2015-0001:1
HHSN268201100005C
692145
IUT20-60
2R01DK075787-06A1
2014-2020.4.01.15-0012 GENTRANSMED
U01AG009740
RC2 AG036495
175.010.2007.006
U01HG004399
CA87969
U01HG004424
EU/QLRT-2001-01254
20070481
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: HERDC Pre-Audit
Queensland Brain Institute Publications
Institute for Molecular Bioscience - Publications
 
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