Late-onset hypogonadism and lifestyle-related metabolic disorders.

Emerging new evidence suggests that metabolic disorders may aggravate LOH effects on the fertility potential of males in reproductive age, by enhancing T deficiency. These results clearly show that metabolic disorders, such as obesity and diabetes, have a greater impact on causing hypogonadotropic hypogonadism than tissue senescence. Further, TRT and off-label alternatives capable of restoring T levels appear as suitable to improve LOH, while also counteracting comorbidities related with metabolic diseases.