Summary
This Mendelian randomisation study of 26,057 mother–offspring pairs from the HUNT cohort challenges the Developmental Origins of Health and Disease hypothesis by finding little evidence that maternal genetic variants influencing offspring birthweight are associated with offspring cardiometabolic risk after adjusting for offspring genetic risk. Instead, offspring genetic risk scores were strongly related to cardiometabolic outcomes independent of maternal genetic influences, suggesting that the intrauterine environment, as proxied by maternal birthweight-associated SNPs, is unlikely to be a major determinant of adverse cardiometabolic outcomes in population-based samples.
UK applicability
The findings are relevant to UK maternal and child health policy and clinical practice, particularly regarding the interpretation of the Developmental Origins hypothesis. If the intrauterine environment (as captured by maternal genetics for birthweight) does not substantially predict offspring cardiometabolic risk, this may reframe public health priorities around maternal nutrition and early life interventions in the UK.
Key measures
Maternal and offspring genetic risk scores (GRS) for birthweight-associated SNPs; offspring cardiometabolic risk factors (as measured in the HUNT Study)
Outcomes reported
The study examined whether maternal genetic variants associated with offspring birthweight predict offspring cardiometabolic risk factors in later life, using genetic risk scores in mother–offspring and father–offspring pairs from the HUNT cohort.
Topic tags
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