ArticleBMC medicine2025
Assessing the causal and independent impact of parity-related reproductive factors on risk of breast cancer subtypes.
Article in BMC medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Evaluation of a National Breast Cancer Screening Program in a Middle-Income Country: The Case of Kazakhstan.International journal of environmental research and public health · 2026Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundObservational evidence proposes a protective effect of having children and an early first pregnancy on breast cancer development; however, the causality of this association remains uncertain. Here, we assess whether parity-related reproductive factors impact breast cancer risk independently of each other and other causally related or genetically correlated factors: adiposity, age at menarche, and age at menopause.
methodsWe used genetic data from UK Biobank for reproductive factors and adiposity, and the Breast Cancer Association Consortium for risk of overall, estrogen receptor (ER) positive and negative breast cancer, and breast cancer subtypes. We applied univariable and multivariable Mendelian randomization (MR) to estimate genetically predicted direct effects of ever parous status, ages at first birth and last birth, and number of births on breast cancer risk.
resultsWe found limited evidence for a genetically predicted protective effect of an earlier age at first birth on breast cancer risk. While the univariable analysis revealed later age at first birth decreased ER-negative breast cancer risk (odds ratio (OR): 0.76; 95% confidence interval: 0.61, 0.95 per standard deviation (SD) increase in age at first birth), this effect attenuated with separate adjustment for age at menarche (potential confounder) (OR: 0.83; 0.62, 1.06) and age at menopause (genetically correlated factor) (OR: 0.80; 0.66, 1.01). Furthermore, we found evidence that a later age at first birth decreased HER2-enriched breast cancer risk but only after adjusting for number of births (potential mediator) (OR: 0.28; 0.11, 0.57 per SD increase in age at first birth). In the multivariable analysis, we found little evidence for genetically predicted effects of ever-parous status, age at last birth, or number of births on breast cancer risk; however, analyses of ever-parous status and age at last birth were limited by weak instruments.
conclusionsThis study found minimal evidence of a genetically predicted protective effect of earlier age at first birth on breast cancer risk, while identifying some evidence for a genetically predicted adverse effect on ER-negative breast cancer risk. However, weak instruments limited the multivariable analysis of ever parous status and age at last birth, which may be improved with larger sample sizes.
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