Maternal and fetal genetic contribution to gestational weight gain
Nicole M. Warrington,
Carol A Wang,
Robin N Beaumont,
Sheila J. Barton,
Anna E Jonsson,
Carla MT Tiesler,
Susan M. Ring,
John W. Holloway,
Vincent W.V. Jaddoe,
William L Lowe,
Andrew T Hattersley,
Ellen Aagard Nohr,
Loreto Santa Marina,
Joachim H Heinrich,
Rebecca M Reynolds,
Olli T. Raitakari,
Hazel M Inskip,
Mariona Bustamante Pineda,
Thorkild IA Sorensen,
Janine F. Felix,
David M Evans,
Debbie A Lawlor,
Early Growth Genetics (EGG) consortium
Posted 14 Mar 2017
bioRxiv DOI: 10.1101/116434 (published DOI: 10.1038/ijo.2017.248)
Posted 14 Mar 2017
Background: Clinical recommendations to limit gestational weight gain (GWG) imply high GWG is causally related to adverse outcomes in mother or offspring, but GWG is the sum of several inter-related complex phenotypes (maternal fat deposition and vascular expansion, placenta, amniotic fluid and fetal growth). Understanding the genetic contribution to GWG could help clarify the potential effect of its different components on maternal and offspring health. Here we explore the genetic contribution to total, early and late GWG. Participants and Methods: A genome-wide association study was used to identify maternal and fetal variants contributing to GWG in up to 10,543 mothers and up to 16,317 offspring of European origin, with replication in 10,660 mothers and 7,561 offspring. Additional analyses determined the proportion of variability in GWG from maternal and fetal common genetic variants and the overlap of established genome-wide significant variants for phenotypes relevant to GWG (e.g. maternal BMI and glucose, birthweight). Results: We found that approximately 20% of the variability in GWG was tagged by common maternal genetic variants, and that the fetal genome made a surprisingly minor contribution to explaining variation in GWG. We were unable to identify any genetic variants that reached genome-wide levels of significance (P<5x10-8) and replicated. Some established maternal variants associated with increased BMI, fasting glucose and type 2 diabetes were associated with lower early, and higher later GWG. Maternal variants related to higher systolic blood pressure were related to lower late GWG. Established maternal and fetal birthweight variants were largely unrelated to GWG. Conclusion: We found a modest contribution of maternal common variants to GWG and some overlap of maternal BMI, glucose and type 2 diabetes variants with GWG. These findings suggest that associations between GWG and later offspring/maternal outcomes may be due to the relationship of maternal BMI and gestational diabetes with GWG.
- Downloaded 266 times
- Download rankings, all-time:
- Site-wide: 77,296 out of 117,931
- In genetics: 3,680 out of 5,127
- Year to date:
- Site-wide: 112,861 out of 117,931
- Since beginning of last month:
- Site-wide: 108,999 out of 117,931
Downloads over time
Distribution of downloads per paper, site-wide
- 27 Nov 2020: The website and API now include results pulled from medRxiv as well as bioRxiv.
- 18 Dec 2019: We're pleased to announce PanLingua, a new tool that enables you to search for machine-translated bioRxiv preprints using more than 100 different languages.
- 21 May 2019: PLOS Biology has published a community page about Rxivist.org and its design.
- 10 May 2019: The paper analyzing the Rxivist dataset has been published at eLife.
- 1 Mar 2019: We now have summary statistics about bioRxiv downloads and submissions.
- 8 Feb 2019: Data from Altmetric is now available on the Rxivist details page for every preprint. Look for the "donut" under the download metrics.
- 30 Jan 2019: preLights has featured the Rxivist preprint and written about our findings.
- 22 Jan 2019: Nature just published an article about Rxivist and our data.
- 13 Jan 2019: The Rxivist preprint is live!