ArticleCommunications biology2024
Disentangling the link between maternal influences on birth weight and disease risk in 36,211 genotyped mother-child pairs.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Maternal and fetal genetic predispositions to insulin deficiency and resistance affect fetal growth through distinct pathways.Diabetologia · 2026Article
- Disentangling the relationship between intrauterine exposures and offspring growth in mid-childhood.BMC medicine · 2026Article
- Genomic approaches to understanding pregnancy phenotypes and birth outcomes and their links with long-term maternal and offspring health-the value of distinguishing maternal and fetal genetic effects.Frontiers in genetics · 2026Review
- Human genetics implicate thromboembolism in the pathogenesis of long COVID in individuals of European ancestry.Nature cardiovascular research · 2025Article
- Intergenerational transmission of complex traits and the offspring methylome.Molecular psychiatry · 2025Article
- Socioeconomic status, individual behaviors and risk for Lymphomas: a Mendelian randomization study.Journal of Cancer · 2024Article
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Authors and funding
4 authors.
Funding
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Abstract
Epidemiological studies have robustly linked lower birth weight to later-life disease risks. These observations may reflect the adverse impact of intrauterine growth restriction on a child's health. However, causal evidence supporting such a mechanism in humans is largely lacking. Using Mendelian Randomization and 36,211 genotyped mother-child pairs from the FinnGen study, we assessed the relationship between intrauterine growth and five common health outcomes (coronary heart disease (CHD), hypertension, statin use, type 2 diabetes and cancer). We proxied intrauterine growth with polygenic scores for maternal effects on birth weight and took into account the transmission of genetic variants between a mother and a child in the analyses. We find limited evidence for contribution of normal variation in maternally influenced intrauterine growth on later-life disease. Instead, we find support for genetic pleiotropy in the fetal genome linking birth weight to CHD and hypertension. Our study illustrates the opportunities that data from genotyped parent-child pairs from a population-based biobank provides for addressing causality of maternal influences.
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