TY - JOUR
T1 - Genotype–covariate interaction effects and the heritability of adult body mass index
JF - Nature Genetics
Y1 - 2017
A1 - Matthew R Robinson
A1 - English, Geoffrey
A1 - Moser, Gerhard
A1 - Lloyd-Jones, Luke R.
A1 - Triplett, Marcus A.
A1 - Zhihong Zhu
A1 - Ilja M Nolte
A1 - Jana V. van Vliet-Ostaptchouk
A1 - Snieder, Harold
A1 - Tõnu Esko
A1 - Lili Milani
A1 - Mägi, Reedik
A1 - Andres Metspalu
A1 - Patrik K E Magnusson
A1 - Nancy L Pedersen
A1 - Ingelsson, Erik
A1 - Johannesson, Magnus
A1 - Yang, Jian
A1 - Cesarini, David
A1 - Peter M Visscher
KW - BMI
KW - Genetics
KW - GWAS
AB - Obesity is a worldwide epidemie, 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 x 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 x 10-5 and LRT = 30.80, P = 1.42 x 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.
VL - 49
IS - 8
JO - Nat Genet
ER -