Purpose of review The prevalence of obesity has risen steadily for the past 35 years and presently affects more than a third of the US population. A concurrent decline in semen parameters has been described, and a growing body of literature suggests that obesity contributes to the male infertility. The purpose of this review is to examine the effects of obesity on male fertility, the mechanisms by which impaired reproductive health arise, and the outcomes of treatment. Recent findings Obesity alters the hypothalamic-pituitary-gonadal axis both centrally and peripherally, resulting in hypogonadotropic, hyperestrogenic hypogonadism. Adipose tissue-derived factors, like leptin and adipokines, regulate testosterone production and inflammation, respectively. Increased systemic inflammation results in increased reactive oxygen species and sperm DNA fragmentation. Increased testicular temperature because of body habitus and inactivity impairs spermatogenesis. The degree to which obesity affects hormone levels, semen parameters, sperm DNA integrity, and pregnancy rates is variable, which may be the result of other comorbid conditions. Treatment in the form of weight loss has also had inconsistent results. Summary Multiple interdependent mechanisms contribute to the detrimental effect of obesity on male fertility. Large, randomized control trials are needed to better characterize the therapeutic benefits of weight loss to restore male reproductive potential.
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