madman
Super Moderator
The single most significant risk factor for testosterone deficiency in men is obesity. The pathophysiological mechanisms involved in male obesity-related secondary hypogonadism are highly complex. Obesity-induced increase in levels of leptin, insulin, proinflammatory cytokines and oestrogen can cause a functional hypogonadotrophic hypogonadism with the defect present at the level of the hypothalamic gonadotrophin-releasing hormone (GnRH) neurons. The resulting hypogonadism by itself can worsen obesity, creating a self perpetuating cycle. Obesity-induced hypogonadism is reversible with substantial weight loss. Lifestyle-measures form the cornerstone of management as they can potentially improve androgen deficiency symptoms irrespective of their effect on testosterone levels. In selected patients, bariatric surgery can reverse the obesity-induced hypogonadism. If these measures fail to relieve symptoms and to normalise testosterone levels, in appropriately selected men, testosterone replacement therapy could be started. Aromatase inhibitors and selective oestrogen receptor modulators are not recommended due to lack of consistent clinical trial-based evidence.
Figure 1: The central regulation of testosterone production in normal individuals and individuals with male obesity-related secondary hypogonadism
Figure 2: The pathophysiological aspects of male obesity-related secondary hypogonadism
Table 1: Recommendations for the diagnosis and management of testosterone deficiency
Summary and conclusions
With the increasing prevalence of obesity, the incidence of MOSH is also increasing. Lifestyle modification remains the first-line management of MOSH as this improves the overall health of the patient and has the potential to improve androgen deficiency symptoms irrespective of any effect on testosterone levels. In selected patients with clinical indications, weight loss interventions such as bariatric surgery can revert the hypogonadotrophic hypogonadism caused by obesity. If these measures fail to relieve symptoms and to normalise testosterone levels, in appropriately selected men, TRT could be started. Other medications such as aromatase inhibitors and selective oestrogen receptor modulators are not recommended due to lack of clinical trial-based evidence.
Figure 1: The central regulation of testosterone production in normal individuals and individuals with male obesity-related secondary hypogonadism
Figure 2: The pathophysiological aspects of male obesity-related secondary hypogonadism
Table 1: Recommendations for the diagnosis and management of testosterone deficiency
Summary and conclusions
With the increasing prevalence of obesity, the incidence of MOSH is also increasing. Lifestyle modification remains the first-line management of MOSH as this improves the overall health of the patient and has the potential to improve androgen deficiency symptoms irrespective of any effect on testosterone levels. In selected patients with clinical indications, weight loss interventions such as bariatric surgery can revert the hypogonadotrophic hypogonadism caused by obesity. If these measures fail to relieve symptoms and to normalise testosterone levels, in appropriately selected men, TRT could be started. Other medications such as aromatase inhibitors and selective oestrogen receptor modulators are not recommended due to lack of clinical trial-based evidence.
