Win Shwe Sin, Sulo Gerhard, Engeland Anders, Klungsøyr Kari
Department of Global Public Health and Primary Care, Faculty of Medicine, University of Bergen, Bergen, Norway.
Department of Chronic Disease, Norwegian Institute of Public Health, Bergen, Norway.
Paediatr Perinat Epidemiol. 2025 Aug;39(6):559-567. doi: 10.1111/ppe.70032. Epub 2025 May 20.
Studies have suggested that men with cardiometabolic conditions may have an increased risk of offspring perinatal mortality. However, this association remains underexplored.
We aimed to study the association between fathers' cardiometabolic conditions and offspring perinatal mortality utilising linked data from national health registries in Norway.
In this population-based cohort study, males registered in the Medical Birth Registry of Norway (MBRN), born 1967-2005, were linked to their singleton offsprings born 2004-2020. The Norwegian Patient Registry and the Norwegian Prescription Database were used to define study exposures: history of hypertension, diabetes, dyslipidaemia, severe obesity or any of these at any time before/during the year of childbirth while fathers having no such conditions were the reference group. Perinatal mortality was defined as foetal death from 16 weeks' gestation or neonatal deaths within the first month after birth (from the MBRN). We fitted multilevel random-intercept Poisson regression models to account for the clustering of infants born to the same father. We reported incidence rate ratio (IRR) with 95% confidence Intervals (CI).
Of 703,746 infants, 3.6% (n = 25,314) were born to fathers with any condition. Overall, 4827 (0.7%) of them died perinatally. In fully adjusted models, infants of fathers with hypertension had a 29% higher risk of dying perinatally (IRR 1.29, 95% CI 1.05, 1.57) relative to those of fathers without cardiometabolic conditions. Effect estimates for paternal diabetes, severe obesity and any condition also indicated a possible increased perinatal mortality associated with these conditions. In the sex-stratified analysis, the associations were stronger in male offspring (IRR 1.29, 95% CI 1.06, 1.58) than female offspring (IRR 1.01, 95% CI 0.78, 1.29).
The increased perinatal mortality in offspring to fathers with cardiometabolic conditions emphasises fathers' biological role in foetal and placental programming and development. Whether offspring sex impacts these associations needs further investigation.
研究表明，患有心脏代谢疾病的男性其后代围产期死亡风险可能会增加。然而，这种关联仍未得到充分研究。
我们旨在利用挪威国家健康登记处的关联数据，研究父亲的心脏代谢疾病与后代围产期死亡之间的关联。
在这项基于人群的队列研究中，将1967年至2005年在挪威医疗出生登记处（MBRN）登记的男性与其2004年至2020年出生的单胎后代进行关联。挪威患者登记处和挪威处方数据库用于定义研究暴露因素：高血压病史、糖尿病、血脂异常、重度肥胖或在分娩当年之前/期间任何时间出现的上述任何一种情况，而没有这些疾病的父亲作为参照组。围产期死亡定义为妊娠16周后的胎儿死亡或出生后第一个月内的新生儿死亡（来自MBRN）。我们采用多水平随机截距泊松回归模型来考虑同一父亲所生孩子的聚类情况。我们报告了发病率比（IRR）及其95%置信区间（CI）。
在703,746名婴儿中，3.6%（n = 25,314）的父亲患有某种疾病。总体而言，其中4827名（0.7%）在围产期死亡。在完全调整模型中，患有高血压的父亲的婴儿围产期死亡风险比没有心脏代谢疾病的父亲的婴儿高29%（IRR 1.29，95% CI 1.05，1.57）。父亲患糖尿病、重度肥胖以及患有任何疾病的效应估计值也表明，这些情况可能会增加围产期死亡风险。在按性别分层分析中，男性后代的关联更强（IRR 1.29，95% CI 1.06，1.58），而女性后代则较弱（IRR 1.01，95% CI 0.78，1.29）。
患有心脏代谢疾病的父亲的后代围产期死亡率增加，这凸显了父亲在胎儿和胎盘编程及发育中的生物学作用。后代性别是否会影响这些关联需要进一步研究。
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