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Mendelian randomization study of maternal influences on birthweight and future cardiometabolic risk in the HUNT cohort

Author

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  • Gunn-Helen Moen

    (Faculty of Medicine, University of Oslo
    The University of Queensland
    NTNU, Norwegian University of Science and Technology
    University of Bristol)

  • Ben Brumpton

    (NTNU, Norwegian University of Science and Technology
    St. Olavs Hospital, Trondheim University Hospital
    Medical Research Council Integrative Epidemiology Unit at the University of Bristol)

  • Cristen Willer

    (University of Michigan
    University of Michigan
    University of Michigan)

  • Bjørn Olav Åsvold

    (NTNU, Norwegian University of Science and Technology
    St. Olavs Hospital, Trondheim University Hospital)

  • Kåre I. Birkeland

    (Faculty of Medicine, University of Oslo)

  • Geng Wang

    (The University of Queensland)

  • Michael C. Neale

    (Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University)

  • Rachel M. Freathy

    (College of Medicine and Health, University of Exeter)

  • George Davey Smith

    (University of Bristol
    Medical Research Council Integrative Epidemiology Unit at the University of Bristol
    Bristol NIHR Biomedical Research Centre)

  • Deborah A. Lawlor

    (University of Bristol
    Medical Research Council Integrative Epidemiology Unit at the University of Bristol
    Bristol NIHR Biomedical Research Centre)

  • Robert M. Kirkpatrick

    (Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University)

  • Nicole M. Warrington

    (The University of Queensland
    NTNU, Norwegian University of Science and Technology
    Medical Research Council Integrative Epidemiology Unit at the University of Bristol)

  • David M. Evans

    (The University of Queensland
    Medical Research Council Integrative Epidemiology Unit at the University of Bristol)

Abstract

There is a robust observational relationship between lower birthweight and higher risk of cardiometabolic disease in later life. The Developmental Origins of Health and Disease (DOHaD) hypothesis posits that adverse environmental factors in utero increase future risk of cardiometabolic disease. Here, we explore if a genetic risk score (GRS) of maternal SNPs associated with offspring birthweight is also associated with offspring cardiometabolic risk factors, after controlling for offspring GRS, in up to 26,057 mother–offspring pairs (and 19,792 father–offspring pairs) from the Nord-Trøndelag Health (HUNT) Study. We find little evidence for a maternal (or paternal) genetic effect of birthweight associated variants on offspring cardiometabolic risk factors after adjusting for offspring GRS. In contrast, offspring GRS is strongly related to many cardiometabolic risk factors, even after conditioning on maternal GRS. Our results suggest that the maternal intrauterine environment, as proxied by maternal SNPs that influence offspring birthweight, is unlikely to be a major determinant of adverse cardiometabolic outcomes in population based samples of individuals.

Suggested Citation

  • Gunn-Helen Moen & Ben Brumpton & Cristen Willer & Bjørn Olav Åsvold & Kåre I. Birkeland & Geng Wang & Michael C. Neale & Rachel M. Freathy & George Davey Smith & Deborah A. Lawlor & Robert M. Kirkpatr, 2020. "Mendelian randomization study of maternal influences on birthweight and future cardiometabolic risk in the HUNT cohort," Nature Communications, Nature, vol. 11(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-19257-z
    DOI: 10.1038/s41467-020-19257-z
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    Cited by:

    1. Tom G. Richardson & Daniel J. M. Crouch & Grace M. Power & Fernanda Morales-Berstein & Emma Hazelwood & Si Fang & Yoonsu Cho & Jamie R. J. Inshaw & Catherine C. Robertson & Carlo Sidore & Francesco Cu, 2022. "Childhood body size directly increases type 1 diabetes risk based on a lifecourse Mendelian randomization approach," Nature Communications, Nature, vol. 13(1), pages 1-9, December.

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