Body Mass Index-Related Alterations in Gonadotropin Secretion Among Women with Polycystic Ovary Syndrome Compared...

To investigate the association between body mass index (BMI) and gonadotropin secretion, including serum luteinizing hormone (LH), follicle-stimulating hormone (FSH), and the LH/FSH ratio, among women with polycystic ovary syndrome (PCOS), and to compare these parameters with healthy women.

This comparative cross-sectional analytical study included 400 women aged 18-35 years recruited from outpatient gynecology and endocrinology clinics at private-sector medical centers in Irbid, Jordan, between June 2025 and April 2026. The study included 200 women diagnosed with PCOS according to the Rotterdam criteria and 200 age-comparable healthy controls. The PCOS group was stratified into four BMI categories (<25, 25-<28, 28-<31, and ≥31 kg/m²), with 50 women in each category. Clinical and anthropometric characteristics were assessed, and serum LH and FSH concentrations were measured. The LH/FSH ratio was calculated for each participant. Differences between groups were evaluated using appropriate statistical tests, while one-way analysis of variance was used to compare PCOS subgroups according to BMI. Pearson's correlation analysis was used to assess associations between BMI and gonadotropin parameters.

The mean age was comparable between women with PCOS and healthy controls (26.31 ± 5.36 vs. 26.47 ± 5.16 years; p = 0.23). Women with PCOS had significantly higher BMI than controls (27.85 ± 3.47 vs. 22.81 ± 2.29 kg/m²; p < 0.001). Among women with PCOS, menstrual irregularity, hirsutism, acne, infertility, and polycystic ovarian morphology were observed in 87.5%, 79.5%, 78.5%, 70.0%, and 100%, respectively. Serum LH was significantly higher in women with PCOS than in controls (8.44 ± 2.61 vs. 6.53 ± 1.16 IU/L; p < 0.001), whereas FSH was significantly lower (4.64 ± 0.98 vs. 7.96 ± 1.18 IU/L; p < 0.001), resulting in a higher LH/FSH ratio (1.84 ± 0.50 vs. 0.83 ± 0.20; p < 0.001). Within the PCOS group, LH progressively decreased across increasing BMI categories, from 11.58 ± 1.26 IU/L in women with BMI < 25 kg/m² to 5.40 ± 1.29 IU/L in those with BMI ≥ 31 kg/m² (p < 0.001). Similarly, the LH/FSH ratio decreased from 2.46 ± 0.18 to 1.28 ± 0.23 across these BMI categories (p < 0.001), whereas FSH did not differ significantly (p = 0.07). BMI showed strong inverse correlations with LH (r = -0.870, p < 0.001) and the LH/FSH ratio (r = -0.869, p < 0.001), but not with FSH (r = -0.126, p = 0.075).

Women with PCOS demonstrated a distinct gonadotropin profile characterized by higher LH and LH/FSH ratio and lower FSH compared with healthy controls. Among women with PCOS, increasing BMI was strongly associated with lower LH concentrations and LH/FSH ratios. These findings highlight the importance of considering BMI when interpreting gonadotropin profiles in PCOS, although prospective studies are required to determine whether changes in body weight directly influence gonadotropin secretion and reproductive outcomes.