There are limited data regarding the fertility outcomes of interventions in men with obesity. Nevertheless, a patient consultation about fertility is an opportunity for a GP to establish a therapeutic relationship with the patient and to promote lifestyle modifications and weight loss that will have long-term cardiovascular benefits. These include tobacco cessation, avoidance of excessive alcohol and promotion of moderate exercise. Identified comorbidities, such as diabetes, dyslipidaemia and OSA, should also be treated. Treatment of OSA with continuous positive airway pressure (CPAP) has been shown to increase testosterone levels.
Weight loss can reverse the hormonal abnormalities seen in overweight men, while also improving comorbidities such as OSA.17 Biochemical changes that correlate with weight loss include increases in serum testosterone and sex hormone binding globulin levels and decreases in oestradiol levels. Nonsurgical approaches to weight loss include low-calorie diets, increased physical exercise and sometimes pharmacological therapy to help maintenance of weight loss. Bariatric surgery allows greater and more sustained weight loss. Reduced BMI in men after bariatric surgery has been shown to improve their sexual desire and satisfaction, as well as erectile function.18
There is emerging evidence to suggest a beneficial effect of weight loss through lifestyle modification on sperm parameters including DNA fragmentation.19 The impact of bariatric surgery is less clear, with some studies demonstrating reduced sperm defragmentation following surgery, whereas others have observed decreased or no impact on sperm concentration and/or motility.20,21
Importantly, the effects of paternal obesity on spermatogenesis are likely to be at most modest, with most male subfertility and significant sperm defects being a result of intrinsic disorders of spermatogenesis rather than solely attributable to BMI. It would thus be remiss to overstate the effects of overweight on fertility and to rely exclusively on weight loss as a cure for subfertility in men with obesity.
Although weight loss improves the hormone profile, there are few data regarding therapies that directly target endocrine abnormalities in men with obesity. Aromatase inhibitors might potentially correct oestrogen excess and ameliorate hypogonadotrophic hypogonadism, but this intervention has not been well studied in men with obesity, and these drugs are not approved for this indication. Notably, even in the presence of hypogonadism, exogenous androgens should not be prescribed in men with obesity seeking fertility because of their contraceptive action.
Other potential therapies include the use of phosphodiesterase inhibitors to improve erectile function. Scrotal lipectomy to remove accumulated fat has been advocated to reduce scrotal temperature.
Male obesity is a significant health issue and is associated with decreased fertility. The association is likely to involve multiple factors, including endocrine dysregulation, reduced sexual desire and function, comorbidities such as OSA, and suboptimal semen parameters. Although there are limited data demonstrating the direct benefits of weight loss on semen parameters and sperm quality, weight loss has been shown to improve the hormone profile and is linked with improved sexual function. Importantly, a consultation about fertility provides a rare opportunity for GPs to engage with men who have obesity about their weight, lifestyle choices and cardiovascular health. Practice points regarding male obesity and fertility are summarised in the Box. MT