Achkar Mariella El, Atieh Ornina, Ghadban Carole, Awad Toufic, Ghadban Elie, Grandjean Valérie, Yarkiner Zalihe, Raad Georges, Khalife Marie-Claude Fadous
School of Medicine and Medical Sciences, Holy Spirit University of Kaslik, Jounieh, Lebanon.
Université Côte d'Azur, Inserm, C3M, Team Control of Gene Expression (10), Nice, France.
Andrology. 2025 Jan;13(1):45-54. doi: 10.1111/andr.13673. Epub 2024 Jun 4.
Congenital urogenital anomalies affect 4-60 per 10,000 births. Maternal obesity, along with other risk factors, is well documented as a contributing factor. However, the impact of paternal obesity on risk is unclear. Obesity is prevalent among men of reproductive age, highlighting the need for further research into the potential association between paternal obesity and offspring congenital urogenital anomalies.
This study aims to determine the association between paternal obesity and the risk of congenital urogenital malformations in offspring.
Case-control study conducted on 179 newborns (91 cases, 88 controls) selected from the Notre Dame des Secours-university hospital database. Cases were identified as newborns presenting at least one congenital urogenital abnormality, defined as developmental anomalies that can result in a variety of malformations affecting the kidneys, ureters, bladder, and urethra. Controls were identified as newborns without any congenital abnormalities. The exclusion criteria were maternal obesity, infections during pregnancy, chronic diseases, prematurity, growth retardation, assisted reproductive technologies for conception, substance abuse, down syndrome, and other malformations. Data were collected through phone interviews, medical records, and questionnaires. In this study, the exposure was the preconceptional paternal body mass index (BMI), which was calculated based on self-reported height and weight. According to guidelines from the US Centers for Disease Control and Prevention (CDC), individuals are considered to be in the healthy weight range if their BMI (kg/m) is between 18.5 and < 25. They are classified as overweight if their BMI is ≥ 25, obese class I if their BMI is between 30 and < 35, obese class II if their BMI is between 35 and < 40, and obese class III if their BMI is 40 or higher. Logistic regression analysis was employed to quantify the association between paternal obesity and urogenital conditions in offspring.
Significant differences in median (minimum-maximum) paternal BMI values were noted between the cases and controls at the time of conception (cases: 27.7 (43-20.1), controls: 24.8 (40.7-19.6); p < 0.0001). Logistic regression analysis confirmed that at the time of conception, compared to normal-weight fathers, overweight fathers displayed a heightened risk of offspring congenital malformations, with an odds ratio (OR) of 4.44 (95% CI = 2.1-9.1). Similarly, fathers categorized as obese Class I at conception had approximately eight times higher odds (OR = 8.62, 95% CI = 2.91-25.52) of having offspring with urogenital conditions compared to normal-weight fathers. Additionally, fathers classified as obese Class II at conception exhibited 5.75 times higher odds (OR = 5.75, 95% CI = 0.96-34.44) of having offspring with urogenital conditions in comparison to normal-weight fathers.
We found that the risk of urogenital malformations increased with paternal BMI during the preconceptional period. The findings suggest the importance of addressing paternal obesity in efforts to reduce the risk of urogenital congenital malformations in offspring.
先天性泌尿生殖系统异常在每10000例出生中影响4 - 60例。母亲肥胖以及其他风险因素,已被充分证明是一个促成因素。然而,父亲肥胖对风险的影响尚不清楚。肥胖在育龄男性中很普遍,这凸显了进一步研究父亲肥胖与后代先天性泌尿生殖系统异常之间潜在关联的必要性。
本研究旨在确定父亲肥胖与后代先天性泌尿生殖系统畸形风险之间的关联。
对从巴黎圣母院救济大学医院数据库中选取的179名新生儿(91例病例,88例对照)进行病例对照研究。病例被确定为至少存在一种先天性泌尿生殖系统异常的新生儿,先天性泌尿生殖系统异常定义为可导致影响肾脏、输尿管、膀胱和尿道的各种畸形的发育异常。对照被确定为无任何先天性异常的新生儿。排除标准包括母亲肥胖、孕期感染、慢性病、早产、生长迟缓、辅助生殖技术受孕、药物滥用、唐氏综合征和其他畸形。数据通过电话访谈、病历和问卷收集。在本研究中,暴露因素是孕前父亲的体重指数(BMI),其根据自我报告的身高和体重计算得出。根据美国疾病控制与预防中心(CDC)的指南,如果个体的BMI(kg/m²)在18.5至<25之间,则被认为处于健康体重范围。如果BMI≥25,则被归类为超重;如果BMI在30至<35之间,则为I级肥胖;如果BMI在35至<40之间,则为II级肥胖;如果BMI为40或更高,则为III级肥胖。采用逻辑回归分析来量化父亲肥胖与后代泌尿生殖系统疾病之间的关联。
在受孕时,病例组和对照组的父亲BMI中位数(最小值 - 最大值)存在显著差异(病例组:27.7(43 - 20.1),对照组:24.8(40.7 - 19.6);p < 0.0001)。逻辑回归分析证实,在受孕时,与体重正常的父亲相比,超重父亲的后代先天性畸形风险增加,优势比(OR)为4.44(95%置信区间 = 2.1 - 9.1)。同样,受孕时被归类为I级肥胖的父亲,其后代患泌尿生殖系统疾病的几率比体重正常的父亲高出约八倍(OR = 8.62,95%置信区间 = 2.91 - 25.52)。此外,受孕时被归类为II级肥胖的父亲,其后代患泌尿生殖系统疾病的几率比体重正常的父亲高出5.75倍(OR = 5.75,95%置信区间 = 0.96 - 34.44)。
我们发现,孕前父亲BMI增加会导致泌尿生殖系统畸形风险上升。这些发现表明,在努力降低后代泌尿生殖系统先天性畸形风险的过程中,解决父亲肥胖问题具有重要意义。