Preconceptional paternal obesity may increase the risk of congenital urogenital anomalies in offspring: A case-control study

Abstract

Background: 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.

Objectives: This study aims to determine the association between paternal obesity and the risk of congenital urogenital malformations in offspring.

Methods: 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/m²) 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.

Results: 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.

Discussion and conclusion: 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.

Keywords: congenital abnormalities; obesity; paternal exposure; urogenital system.

FIGURE 1

The study design and flow diagram for the present case–control study. (A) A case–control study was conducted to investigate the association between paternal body mass index (BMI) and the risk of adverse birth outcomes. The study included 179 newborns, with cases (n = 91) and controls (n = 88) selected from the Notre Dame des Secours–University hospital database. Exclusion criteria were applied to ensure that the study population was free of 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. Paternal BMI was calculated and used as the exposure variable in the analysis. The study design was approved by the relevant institutional review board, and all participants provided informed consent. (B) Flow diagram illustrating the screening process and participant selection for the study. Out of the initial 280 files screened, 131 cases and 149 controls were identified. Following the application of inclusion and exclusion criteria, as well as removal of files with missing parental data or refusal to participate (40 cases and 61 controls), the final sample comprised 179 files. This sample consisted of 91 neonates with congenital urogenital abnormalities and 88 neonates without these abnormalities.