madman
Super Moderator
Summary
Obesity prevalence, particularly in children and young adults, is perilously increasing worldwide foreseeing serious negative health impacts in the future to come. Obesity is linked to impaired male gonadal function and is currently a major cause of hypogonadism. Besides signs and symptoms directly derived from decreased circulating testosterone levels, males with obesity also present poor fertility outcomes, further evidencing the parallelism between obesity and male reproductive function. In addition, males with androgen deficiency also exhibit increased fat accumulation and reduced muscle and mineral bone mass. Thus, compelling evidence highlights a vicious cycle where male hypogonadism can lead to increased adiposity, while obesity can be a cause for male hypogonadism. On the opposite direction, sustained weight loss can attain amelioration of male gonadal function. In this scenario, a thorough evaluation of gonadal function in men with obesity is crucial to dissect the causes from the consequences in order to target clinical interventions towards maximized improvement of reproductive health. This review will address the causes and consequences of the bidirectional relationship between obesity and hypogonadism, highlighting the implicit male reproductive repercussions.
CONCLUSION
As obesity prevalence increases worldwide, so does the prevalence of worrisome comorbidities increases. Obesity‐related hypogonadism is an emerging condition that affects the quality of life, disrupts several metabolic functions, and limits male reproductive potential by impairing sexual function and reducing fertility. Moreover, as obesity in young men increases, obesity‐related male infertility is likely to become a serious health issue in the near future. In addition, obesity and male hypogonadism are intimately related in a manner that one condition perpetuates the other. Despite the bidirectional relationship between obesity and male hypogonadism, breaking the vicious cycle is undoubtedly achievable, as sustained weight loss allows the reversal of the negative effects of obesity on reproductive function. These data confer obesity treatment an imperative status, which can span from lifestyle modifications, including caloric‐restriction and increased physical activity as the backbone of any weight loss intervention, to pharmacological therapy or even bariatric surgery, according to the severity of obesity. Nevertheless, further studies are still needed to elucidate the molecular mechanisms behind the vicious cycle of obesity and HPT axis dysfunction. Novel data will then prompt the development of new and more effective interventions and drug therapies in order to dismiss this cycle and achieve optimal clinical outcomes for men with obesity with gonadal and reproductive dysfunction.
Obesity prevalence, particularly in children and young adults, is perilously increasing worldwide foreseeing serious negative health impacts in the future to come. Obesity is linked to impaired male gonadal function and is currently a major cause of hypogonadism. Besides signs and symptoms directly derived from decreased circulating testosterone levels, males with obesity also present poor fertility outcomes, further evidencing the parallelism between obesity and male reproductive function. In addition, males with androgen deficiency also exhibit increased fat accumulation and reduced muscle and mineral bone mass. Thus, compelling evidence highlights a vicious cycle where male hypogonadism can lead to increased adiposity, while obesity can be a cause for male hypogonadism. On the opposite direction, sustained weight loss can attain amelioration of male gonadal function. In this scenario, a thorough evaluation of gonadal function in men with obesity is crucial to dissect the causes from the consequences in order to target clinical interventions towards maximized improvement of reproductive health. This review will address the causes and consequences of the bidirectional relationship between obesity and hypogonadism, highlighting the implicit male reproductive repercussions.
CONCLUSION
As obesity prevalence increases worldwide, so does the prevalence of worrisome comorbidities increases. Obesity‐related hypogonadism is an emerging condition that affects the quality of life, disrupts several metabolic functions, and limits male reproductive potential by impairing sexual function and reducing fertility. Moreover, as obesity in young men increases, obesity‐related male infertility is likely to become a serious health issue in the near future. In addition, obesity and male hypogonadism are intimately related in a manner that one condition perpetuates the other. Despite the bidirectional relationship between obesity and male hypogonadism, breaking the vicious cycle is undoubtedly achievable, as sustained weight loss allows the reversal of the negative effects of obesity on reproductive function. These data confer obesity treatment an imperative status, which can span from lifestyle modifications, including caloric‐restriction and increased physical activity as the backbone of any weight loss intervention, to pharmacological therapy or even bariatric surgery, according to the severity of obesity. Nevertheless, further studies are still needed to elucidate the molecular mechanisms behind the vicious cycle of obesity and HPT axis dysfunction. Novel data will then prompt the development of new and more effective interventions and drug therapies in order to dismiss this cycle and achieve optimal clinical outcomes for men with obesity with gonadal and reproductive dysfunction.
