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Background The relative contribution of maternal and paternal preconceptional cardiometabolic conditions (CMCs) on offspring perinatal mortality remains unclear. This study aimed to compare associations between parental preconceptional CMCs and perinatal mortality in mother-offspring and father-offspring pairs. We also explored the mediating role of placental pregnancy complications in both maternal and paternal associations. Methods We linked individuals born in Norway (1967–2005) to their first singleton offspring born 2005–2020 using data from the Medical Birth Registry of Norway. Preconceptional CMCs (hypertension, diabetes, dyslipidaemia, severe obesity, and any combination of these) were identified using the Norwegian Patient Registry and the Norwegian Prescription Database. Parents without CMCs served as the reference group. Perinatal mortality was defined as foetal death from 16 weeks’ gestation or neonatal death within the first month of life. Relative risks (RR) and 95% confidence intervals (CI) were estimated using log-linear regression models. Causal mediation analyses were conducted within a counterfactual framework. Results We analysed 293,654 mother-offspring and 289,608 father-offspring pairs. Among these, 4.7% of mothers and 2.8% of fathers had at least one preconceptional CMC. Offspring of parents with any CMC had increased perinatal mortality risks compared to those without, independent of parental age, socioeconomic status, or partner’s health. Maternal associations were stronger than paternal associations [e.g., any CMC: RR mothers 2.13 (1.81, 2.49); RR fathers 1.29 (1.02, 1.64)]. Placentally linked pregnancy complications mediated a larger proportion of maternal than paternal associations. Conclusion Both maternal and paternal preconceptional CMCs were associated with increased perinatal mortality. While maternal effects were stronger, paternal health also played a significant role. This underscores the importance of considering paternal CMCs in preconceptional and antenatal care. The lower mediation via placental complications in fathers suggests alternative biological or environmental mechanisms.
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Win et al. (2026) studied this question.
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