Age at Menarche and Coronary Artery Disease Risk: Divergent Associations With Different Sources of Variation
Authors' conclusion
These results are consistent with earlier AAM causally increasing risk of CAD but suggest that later AAM itself does not cause increased risk of CAD; rather, sources of variation in AAM other than common genetic variants can cause both later AAM and increased risk of CAD. Dysglycemia, dyslipidemia, and central adiposity are candidate mediators of the association of later AAM with increased risk of CAD.
Study context
- Population
- Women in the UK Biobank (primary) and the Women's Genome Health Study (validation)UK Biobank
- Participants
- 201,037 women
- Exposure
- Genetically predicted age at menarche (AAM) vs polygenic score (PGS)-adjusted AAM in relation to coronary artery disease (CAD) and CAD risk factors
- Outcome
- Relationship of AAM sources of variation with CAD and CAD risk factors
Methodological detailscohort analysis with polygenic score, UK Biobank primary analysis, validation in Women's Genome Health Study, logistic and linear regression with linear splines
- Cohort analysis with polygenic score
- UK Biobank primary analysis
- Validation in Women's Genome Health Study
- Logistic and linear regression with linear splines
Main finding
As reported in the abstract
CAD and CAD risk factors
- Genetically predicted AAM: linear or roughly linear relationships with CAD and CAD risk factors
- PGS-adjusted AAM: U-shaped relationship with CAD, HbA1c, TG, HDL-C and WHR
Observational data: associations, not effects.
Original publication
Age at Menarche and Coronary Artery Disease Risk: Divergent Associations With Different Sources of Variation. J Clin Endocrinol Metab. Published 10 March 2025. doi:10.
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