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

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. Kirkpatrick, Nicole M. Warrington and David M. Evans ()
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Gunn-Helen Moen: Faculty of Medicine, University of Oslo
Ben Brumpton: NTNU, Norwegian University of Science and Technology
Cristen Willer: University of Michigan
Bjørn Olav Åsvold: NTNU, Norwegian University of Science and Technology
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
Deborah A. Lawlor: University of Bristol
Robert M. Kirkpatrick: Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University
Nicole M. Warrington: The University of Queensland
David M. Evans: The University of Queensland

Nature Communications, 2020, vol. 11, issue 1, 1-12

Abstract: 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.

Date: 2020
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DOI: 10.1038/s41467-020-19257-z

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