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Purpose of review To review the evidence regarding a decrease in worldwide sperm parameters and discuss potential causative factors. Recent findings The topic of worldwide decline in sperm parameters is contentious; however, recent high-quality studies have demonstrated that there is indeed a decline in sperm parameters. Several retrospective and basic science studies have shown possible links for this decline in sperm parameters such as obesity, diet, and environmental toxins. Summary There exist substantial data to suggest a decline in sperm counts over time. Although causative factors have yet to be fully elucidated, potential causes include, increased rates of obesity, poor diet, and exposure to environmental toxins. How this decline in sperm counts reflects fertility has yet to be determined. As such, further studies are necessary to evaluate whether this decline in sperm count correlates with decreased fecundity and how to identify and mitigate potential causative factors.

IMPORTANCE The opportunity to discuss fertility preservation is essential for patients of reproductive age with newly diagnosed cancer before the initiation of treatment. OBJECTIVE To identify factors associated with fertility preservation counseling among patients of reproductive age before initiating chemotherapy. DESIGN, SETTING, AND PARTICIPANTS This cross-sectional study used data obtained from the American Society of Clinical Oncology (ASCO) Quality Oncology Practice Initiative, an oncologist-led quality assessment program that surveys approximately 400 oncology practices biannually, from January, 2015, to June, 2019. MAIN OUTCOMES AND MEASURES The primary outcome was whether reproductive risks were discussed before initiation of chemotherapy. Multivariate logistic regression was performed to identify factors associated with fertility preservation counseling, controlling for age, sex, race/ ethnicity, cancer type, year of study, region, clinic type (academic vs private), annual clinic volume, and rates of insurance coverage. RESULTS Among the 6976 patients of reproductive age (3571 men [51%]; mean (SD) age, 42.5 [7.1] years), with reproductive age ranging from 18 to 40 years for 3405 women and from 18 to 50 years for 3571 men, clinics reported that 3036 of 6976 patients (44%) received counseling regarding the risk of infertility associated with chemotherapy. Women were more likely to be informed (1912 of 3405 [56%]) compared with men (1126 of 3571 [32%]) (P < .001). Factors associated with reduced likelihood of fertility risk discussion included male sex (odds ratio [OR], 0.73; 95% CI, 0.60-0.90), increasing age (OR, 0.93; 95% CI, 0.92-0.94), private practice setting (OR, 0.70; 95% CI, 0.53-0.93), and lack of multidisciplinary team planning (OR, 0.54; 95% CI, 0.41-0.70). Factors associated with increased likelihood of fertility risk discussion included having breast cancer (OR, 1.39; 95% CI,

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Male hypogonadism, the clinical syndrome with variable symptoms associated with gonadal dysfunction, can affect men of all ages. In older males, physiologic changes of the aging testis, account for the majority of decreased testosterone levels in this population. For younger males and adolescents, the etiology of hypogonadism is commonly due to congenital or acquired conditions that disrupt the testis production of testosterone or signaling from the hypothalamic-pituitary-gonadal axis. Diagnosis of hypogonadism in younger males can be a challenge, as symptoms such as decreased libido or erectile dysfunction, common in the older men, are not usually present, and young men instead commonly complain of low energy. While an underlying congenital cause should always be considered in young men with hypogonadism, acquired conditions such as obesity, diabetes, anabolic steroid or illicit drug use have all been associated with low testosterone levels. Outside of modifying identifiable risk factors for hypogonadism, pharmacologic testosterone therapy can also lead to therapeutic dilemmas in young men who desire paternity. Topical or injectable administration of testosterone, through negative feedback on the hypothalamus and pituitary, can decrease spermatogenesis, posing an infertility risk. Other agents that can replace testosterone or increase the body's natural production of testosterone without decreasing spermatogenesis are preferred, such as intranasal testosterone, selective estrogen modulators, aromatase inhibitors or human-chorionic gonadotrophin, often used in combination. Clinicians must maintain a high level of suspicion to properly diagnose young men with hypogonadism and tailor treatment based on both the underlying etiology and fertility goals.