ArticleNature communications2020
Mendelian randomization study of maternal influences on birthweight and future cardiometabolic risk in the HUNT cohort.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 6 of them syntheses that pooled it.
What it found
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The trial behind it
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Who cites it
42 citing papers in PubMed, 6 syntheses or guidelines pooled it, 89 citations in OpenAlex.
- Lifecourse genome-wide association study meta-analysis refines the critical life stages for adiposity's influence on breast cancer risk.Science advances · 2026Pooled it
- Maternal obesity and offspring cardiovascular remodelling - the effect of preconception and antenatal lifestyle interventions: a systematic review.International journal of obesity (2005) · 2024Pooled it
- Methodological approaches, challenges, and opportunities in the application of Mendelian randomisation to lifecourse epidemiology: A systematic literature review.European journal of epidemiology · 2024Pooled it
- Effect of common pregnancy and perinatal complications on offspring metabolic traits across the life course: a multi-cohort study.BMC medicine · 2023Pooled it
- Childhood body size directly increases type 1 diabetes risk based on a lifecourse Mendelian randomization approach.Nature communications · 2022Pooled it
- Genetic meta-analysis of twin birth weight shows high genetic correlation with singleton birth weight.Human molecular genetics · 2021Pooled it
- DNA methylation informs adult cardiovascular risk and prevention for low birthweight individuals.Journal of global health · 2026Article
- Birthweight phenotype genotype mismatch in cardiometabolic programming.Communications medicine · 2026Article
- Disentangling the relationship between intrauterine exposures and offspring growth in mid-childhood.BMC medicine · 2026Article
- Life-course influence of birthweight and subsequent pathways on healthy aging: a Mendelian randomization study.BMC medicine · 2026Article
- A structural mean modeling Mendelian randomization approach to investigate the lifecourse effect of adiposity: applied and methodological considerations.American journal of epidemiology · 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
- Mendelian randomization analyses support causal relationships between unswitched memory B cells and lung squamous cell carcinoma.Discover oncology · 2025Article
- Causal association between EBV and gastritis, gastric cancer, and gastric ulcer: a two-sample Mendelian randomization study.Scientific reports · 2025Article
- Investigating the Relationship Between Maternal Smoking During Pregnancy and Offspring Handedness: Extending the Proxy Gene-by-Environment Mendelian Randomization Study Design to Include Polygenic Risk Scores.Behavior genetics · 2025Article
- The genetics of low and high birthweight and their relationship with cardiometabolic disease.Diabetologia · 2025Article
- Woolf et al's "GWAS by subtraction" is not useful for cross-generational Mendelian randomization studies.BMC research notes · 2025Article
- Parental obesity predisposes male and female offspring to exacerbated cardiac dysfunction and increased mortality after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2025Article
- Gut microbiota in dysmenorrhea: causal evidence from Mendelian randomization and microbial-targeted intervention validation.Frontiers in microbiology · 2025Article
- Exploring and Accounting for Genetically Driven Effect Heterogeneity in Mendelian Randomization.Genetic epidemiology · 2025Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 4 countries.
Funding
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.
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