With the advances in technology that revolutionize everyday lifestyles and industrialization all around the world, obesity has become a modern-day global pandemic. Moreover, as obesity is predicted to reach record numbers in the near future and fertility rates continue to plummet, scientists have began to link the two together. They have revealed that as much as half of all fertility problems come from male-factor defects.
Many researchers have pointed to the increased adipocyte accumulation to generate ROS that propagate systemic and detrimental effects on male reproductive health, while others have attributed the abnormal hormonal profile as the central factor. It appears to be a complex composition of both and, in fact, the increase in adipose-derived hormones and adipokine levels may better explain the association of BMI, altered sperm parameters, and infertility. Recent studies have began to examine genetic biomarkers, an excess of adipose-derived hormones, adipokine release as well as OS. It is suggested that the consistent decrease in hormonal levels and specific proteomic sperm mutations observed in obese males may adversely impact spermatogenesis. Hence, these markers would in turn hinder normal sperm production, maturation and quality, accounting for some of the male-factor defects related to obesity.
The inconsistency in the results from studies demonstrates the necessity for further investigation when examining the effects of obesity on semen parameters. The numerous signs of decreased testosterone levels from excess fat accumulation pose attention for additional focus and study in understanding the overall mechanistic pathway in order to make a definitive link to male infertility.
Simple lifestyle changes have shown to benefit hormonal levels, yet effective treatments, proper lifestyle changes, and surgical options should be further explored. Since antioxidants have been shown to reduce ROS levels, thereby minimizing damage via OS, and have become a hot topic in possibly treatming infertility, this natural remedy should be further explored as a potential treatment for obesity-related male infertility. Additionally, standard and accurate measurements to qualify an individual as obese should be established to confirm the links made to infertility and the health problems that accompany the condition. Nevertheless, the continuing rise and prevalence of both obesity and declining semen quality all over the world, both of which are associated to ROS, call for additional research and a greater awareness to obesity as a potential etiology of male infertility.
Acknowledgment The authors are grateful for the research support from the Center for Reproductive Medicine at Cleveland Clinic.
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