Publication

Genome-wide association studies and Mendelian randomization analyses for leisure sedentary behaviours

van de Vegte, Y. J., Said, M. A., Rienstra, M., van der Harst, P. & Verweij, N., 21-Apr-2020, In : Nature Communications. 11, 1, 10 p., 1770.

Research output: Contribution to journalArticleAcademicpeer-review

APA

van de Vegte, Y. J., Said, M. A., Rienstra, M., van der Harst, P., & Verweij, N. (2020). Genome-wide association studies and Mendelian randomization analyses for leisure sedentary behaviours. Nature Communications, 11(1), [1770]. https://doi.org/10.1038/s41467-020-15553-w

Author

van de Vegte, Yordi J ; Said, M Abdullah ; Rienstra, Michiel ; van der Harst, Pim ; Verweij, Niek. / Genome-wide association studies and Mendelian randomization analyses for leisure sedentary behaviours. In: Nature Communications. 2020 ; Vol. 11, No. 1.

Harvard

van de Vegte, YJ, Said, MA, Rienstra, M, van der Harst, P & Verweij, N 2020, 'Genome-wide association studies and Mendelian randomization analyses for leisure sedentary behaviours', Nature Communications, vol. 11, no. 1, 1770. https://doi.org/10.1038/s41467-020-15553-w

Standard

Genome-wide association studies and Mendelian randomization analyses for leisure sedentary behaviours. / van de Vegte, Yordi J; Said, M Abdullah; Rienstra, Michiel; van der Harst, Pim; Verweij, Niek.

In: Nature Communications, Vol. 11, No. 1, 1770, 21.04.2020.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

van de Vegte YJ, Said MA, Rienstra M, van der Harst P, Verweij N. Genome-wide association studies and Mendelian randomization analyses for leisure sedentary behaviours. Nature Communications. 2020 Apr 21;11(1). 1770. https://doi.org/10.1038/s41467-020-15553-w


BibTeX

@article{2c12773bbb27423a9d4d4ed22e1bc26b,
title = "Genome-wide association studies and Mendelian randomization analyses for leisure sedentary behaviours",
abstract = "Leisure sedentary behaviours are associated with increased risk of cardiovascular disease, but whether this relationship is causal is unknown. The aim of this study is to identify genetic determinants associated with leisure sedentary behaviours and to estimate the potential causal effect on coronary artery disease (CAD). Genome wide association analyses of leisure television watching, leisure computer use and driving behaviour in the UK Biobank identify 145, 36 and 4 genetic loci (P < 1×10−8), respectively. High genetic correlations are observed between sedentary behaviours and neurological traits, including education and body mass index (BMI). Two-sample Mendelian randomization (MR) analysis estimates a causal effect between 1.5 hour increase in television watching and CAD (OR 1.44, 95%CI 1.25–1.66, P = 5.63 × 10−07), that is partially independent of education and BMI in multivariable MR analyses. This study finds independent observational and genetic support for the hypothesis that increased sedentary behaviour by leisure television watching is a risk factor for CAD.",
keywords = "LD SCORE REGRESSION, PHYSICAL-ACTIVITY, RECEPTOR GENE, TIME, ADULTS, MORTALITY, DISEASES, RISK",
author = "{van de Vegte}, {Yordi J} and Said, {M Abdullah} and Michiel Rienstra and {van der Harst}, Pim and Niek Verweij",
year = "2020",
month = apr,
day = "21",
doi = "10.1038/s41467-020-15553-w",
language = "English",
volume = "11",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "Nature Publishing Group",
number = "1",

}

RIS

TY - JOUR

T1 - Genome-wide association studies and Mendelian randomization analyses for leisure sedentary behaviours

AU - van de Vegte, Yordi J

AU - Said, M Abdullah

AU - Rienstra, Michiel

AU - van der Harst, Pim

AU - Verweij, Niek

PY - 2020/4/21

Y1 - 2020/4/21

N2 - Leisure sedentary behaviours are associated with increased risk of cardiovascular disease, but whether this relationship is causal is unknown. The aim of this study is to identify genetic determinants associated with leisure sedentary behaviours and to estimate the potential causal effect on coronary artery disease (CAD). Genome wide association analyses of leisure television watching, leisure computer use and driving behaviour in the UK Biobank identify 145, 36 and 4 genetic loci (P < 1×10−8), respectively. High genetic correlations are observed between sedentary behaviours and neurological traits, including education and body mass index (BMI). Two-sample Mendelian randomization (MR) analysis estimates a causal effect between 1.5 hour increase in television watching and CAD (OR 1.44, 95%CI 1.25–1.66, P = 5.63 × 10−07), that is partially independent of education and BMI in multivariable MR analyses. This study finds independent observational and genetic support for the hypothesis that increased sedentary behaviour by leisure television watching is a risk factor for CAD.

AB - Leisure sedentary behaviours are associated with increased risk of cardiovascular disease, but whether this relationship is causal is unknown. The aim of this study is to identify genetic determinants associated with leisure sedentary behaviours and to estimate the potential causal effect on coronary artery disease (CAD). Genome wide association analyses of leisure television watching, leisure computer use and driving behaviour in the UK Biobank identify 145, 36 and 4 genetic loci (P < 1×10−8), respectively. High genetic correlations are observed between sedentary behaviours and neurological traits, including education and body mass index (BMI). Two-sample Mendelian randomization (MR) analysis estimates a causal effect between 1.5 hour increase in television watching and CAD (OR 1.44, 95%CI 1.25–1.66, P = 5.63 × 10−07), that is partially independent of education and BMI in multivariable MR analyses. This study finds independent observational and genetic support for the hypothesis that increased sedentary behaviour by leisure television watching is a risk factor for CAD.

KW - LD SCORE REGRESSION

KW - PHYSICAL-ACTIVITY

KW - RECEPTOR GENE

KW - TIME

KW - ADULTS

KW - MORTALITY

KW - DISEASES

KW - RISK

U2 - 10.1038/s41467-020-15553-w

DO - 10.1038/s41467-020-15553-w

M3 - Article

C2 - 32317632

VL - 11

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

IS - 1

M1 - 1770

ER -

ID: 123366832