Diminished paternity and gonadal function with increasing obesity in men

Objective: To examine the relationship of male obesity and reproductive function. Design: Observational study. Setting: Academic medical center. Patient(s): Eighty-seven adult men, body mass index (BMI) range from 16.1 to 47.0 kg/m² (mean = 29.3 kg/m²; SD = 6.5 kg/m²). Intervention(s): None. Main Outcome Measure(s): Reproductive history, physical examination, inhibin B, FSH, LH, T, and unbound T levels, and semen analysis. Result(s): Body mass index was negatively correlated with testosterone (r = -0.38), FSH (r = -0.22), and inhibin B levels (r = -0.21) and was positively correlated with E₂ levels (r = 0.34). Testosterone also negatively correlated with skinfold thickness (r = -0.30). There was no correlation of BMI or skinfold thickness with semen analysis parameters (sperm density, volume, motility, or morphology). Inhibin B level correlated significantly with sperm motility (r = 0.23). Men with paternity had lower BMIs (28.0 kg/m² vs. 31.6 kg/m²) and lower skinfold thickness (24.7 mm vs. 34.1 mm) than men without. Conclusion(s): Obesity is an infertility factor in otherwise normal men. Obese men demonstrate a relative hypogonadotropic hypogonadism. Reduced inhibin B levels and diminished paternity suggest compromised reproductive capacity in this population.