Obesity and Male Infertility
Obesity and Male Infertility
Obesity in men is associated with infertility in numerous studies, and the temporal trend for a decline in semen parameters parallels the increasing prevalence of obesity in the developed world. In addition to impaired semen quality, fertility among obese men may be affected by decreased libido and erectile dysfunction. This spectrum of expression of hypogonadism among obese men originates from multiple interacting factors including reduced levels of gonadotropins and testosterone, altered androgen-to-estrogen ratios, insulin resistance, and sleep apnea. No evidence-based treatment that increases the likelihood of pregnancy for the infertility associated with male obesity has been demonstrated to date. Interventions associated with improvement of intermediate outcomes that include the endocrine profile, semen parameters, and sexual function may be appropriately selected based on history, physical findings, as well as endocrine and metabolic evaluation. Among these interventions are weight loss through lifestyle change, relief from sleep apnea, use of aromatase inhibitors, gonadotropin administration, phosphodiesterase inhibitors, and insulin-sensitizing agents.
Infertility, defined as the absence of pregnancy after 1 year of unprotected intercourse, affects 1 in every 13 couples in the United States. Male factor infertility constitutes 25 to 30% of all cases of infertility and contributes, in combination with female factors, to another 30%. Recognized etiologies of male infertility include cryptorchidism, testicular torsion or trauma, varicocele, seminal tract infections, antisperm antibodies, hypogonadotropic hypogonadism, gonadal dysgenesis, and obstruction of the reproductive channels. In case of presumed male factor infertility, couples are often offered intrauterine inseminations (IUIs) or in vitro fertilization (IVF) with intracytoplasmic sperm injection (ICSI). These therapies are expensive and can be beyond the reach of many affected couples.
Simple, inexpensive, and effective therapeutic interventions for male infertility are needed. Potentially effective candidates for intervention include dietary changes and lifestyle modifications. Such interventions gain more importance in light of reports that, paralleling the population body mass index (BMI) increase, the prevalence of male infertility is increasing as evidenced by decreasing sperm counts throughout the world over the last few decades. It has been estimated that sperm counts have fallen by as much as 1.5% each year in the United States, a finding also noted in other Western nations.
Multiple explanations have been proposed for the decline in male fertility including increased prevalence of obesity and exposure to environmental pollution during fetal or adult life. It is known that the prevalence of obesity is increasing in the United States and abroad. In the period from 1991 to 1998, the prevalence of obesity increased from 12 to 17.9% in the general population and from 11.7 to 17.9% in men. Hedley et al estimated the current prevalence of obesity at 30.6%. Multiple reports have described the effect of obesity on male fertility. This effect is thought to be multifactorial and may be modulated by genetic and environmental influences.
This article recapitulates the studies describing the effect of obesity on male fertility, discusses the proposed pathophysiological mechanisms underlying this relation, and suggests, based on the current evidence, a practical approach to evaluate and treat the obese subfertile man.
Abstract and Introduction
Abstract
Obesity in men is associated with infertility in numerous studies, and the temporal trend for a decline in semen parameters parallels the increasing prevalence of obesity in the developed world. In addition to impaired semen quality, fertility among obese men may be affected by decreased libido and erectile dysfunction. This spectrum of expression of hypogonadism among obese men originates from multiple interacting factors including reduced levels of gonadotropins and testosterone, altered androgen-to-estrogen ratios, insulin resistance, and sleep apnea. No evidence-based treatment that increases the likelihood of pregnancy for the infertility associated with male obesity has been demonstrated to date. Interventions associated with improvement of intermediate outcomes that include the endocrine profile, semen parameters, and sexual function may be appropriately selected based on history, physical findings, as well as endocrine and metabolic evaluation. Among these interventions are weight loss through lifestyle change, relief from sleep apnea, use of aromatase inhibitors, gonadotropin administration, phosphodiesterase inhibitors, and insulin-sensitizing agents.
Introduction
Infertility, defined as the absence of pregnancy after 1 year of unprotected intercourse, affects 1 in every 13 couples in the United States. Male factor infertility constitutes 25 to 30% of all cases of infertility and contributes, in combination with female factors, to another 30%. Recognized etiologies of male infertility include cryptorchidism, testicular torsion or trauma, varicocele, seminal tract infections, antisperm antibodies, hypogonadotropic hypogonadism, gonadal dysgenesis, and obstruction of the reproductive channels. In case of presumed male factor infertility, couples are often offered intrauterine inseminations (IUIs) or in vitro fertilization (IVF) with intracytoplasmic sperm injection (ICSI). These therapies are expensive and can be beyond the reach of many affected couples.
Simple, inexpensive, and effective therapeutic interventions for male infertility are needed. Potentially effective candidates for intervention include dietary changes and lifestyle modifications. Such interventions gain more importance in light of reports that, paralleling the population body mass index (BMI) increase, the prevalence of male infertility is increasing as evidenced by decreasing sperm counts throughout the world over the last few decades. It has been estimated that sperm counts have fallen by as much as 1.5% each year in the United States, a finding also noted in other Western nations.
Multiple explanations have been proposed for the decline in male fertility including increased prevalence of obesity and exposure to environmental pollution during fetal or adult life. It is known that the prevalence of obesity is increasing in the United States and abroad. In the period from 1991 to 1998, the prevalence of obesity increased from 12 to 17.9% in the general population and from 11.7 to 17.9% in men. Hedley et al estimated the current prevalence of obesity at 30.6%. Multiple reports have described the effect of obesity on male fertility. This effect is thought to be multifactorial and may be modulated by genetic and environmental influences.
This article recapitulates the studies describing the effect of obesity on male fertility, discusses the proposed pathophysiological mechanisms underlying this relation, and suggests, based on the current evidence, a practical approach to evaluate and treat the obese subfertile man.