Association of Obesity, Inflammation, and Hypogonadism: A Cross-Sectional Study in Males Under 60 Years of Age.

Background Obesity is a significant global health issue closely associated with numerous metabolic disorders, including hypogonadism. Male obesity-related secondary hypogonadism (MOSH) is characterized by reduced testosterone levels, leading to various health complications. The bidirectional relationship between obesity and hypogonadism creates a vicious cycle, with obesity exacerbating hypogonadism and hypogonadism contributing to further obesity. Chronic inflammation, indicated by elevated C-reactive protein (CRP) levels, plays a crucial role in this interplay. The primary aim of this study is to investigate the role of obesity as an isolated factor contributing to hypogonadism. Materials and methods This observational, cross-sectional study was conducted from September 2022 to July 2024 at Dr. D.Y. Patil Medical College and Hospitals in Pune, India. A total of 80 male participants, all under 60 years of age with a BMI greater than 25 kg/m², were included in the study and classified as overweight or obese according to WHO criteria. Exclusion criteria included diabetes, age over 60 years, a BMI less than 25 kg/m², any testicular pathologies, and significant risk factors. After obtaining informed consent, participants underwent thorough clinical examinations and laboratory investigations. Patients who met the criteria were included in the study, with measurements taken for central obesity (waist circumference (WC) and waist-hip ratio (WHR)) and BMI. CRP levels were measured as an inflammatory marker indicative of chronic disease states. Statistical analyses, including correlation and regression analyses, were performed using SPSS software, version 22 (IBM SPSS Statistics, Version 22). Statistical significance was set at p < 0.05. Results The majority of participants fell within the 50-59 age group, with a mean age of 45.95 years. The study found strong positive correlations between BMI (r = 0.76), WC (r = 0.81), and WHR (r = 0.78) with CRP levels, indicating that central obesity is closely linked to systemic inflammation. Additionally, there were significant negative correlations between free testosterone and these anthropometric measures: BMI (r = -0.65), WC (r = -0.70), and WHR (r = -0.67), suggesting that increased adiposity is associated with lower testosterone levels. The strongest negative correlation observed was between CRP and free testosterone (r = -0.82), highlighting the impact of chronic inflammation on hypogonadism. Regression analysis further confirmed that CRP was a significant predictor of free testosterone levels (R-squared = 0.674), emphasizing the crucial role of inflammation in the pathophysiology of hypogonadism in obese individuals. Conclusion This study underscores the intricate relationship between obesity, chronic inflammation, and hypogonadism in men. The bidirectional nature of this relationship suggests that managing obesity and reducing systemic inflammation could potentially alleviate hypogonadism. Interventions focusing on weight loss, improving insulin sensitivity, and anti-inflammatory treatments may thus hold promise in restoring normal testosterone levels in obese men. Understanding and addressing the impact of obesity on male reproductive health is crucial, given the rising prevalence of obesity worldwide. Future research should explore therapeutic avenues and further elucidate the underlying mechanisms of this complex interplay.