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

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/m(2)) 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.