Clinically, infertility is defined as the inability to conceive after a certain period. In contrast, sterility is defined as the inability to produce a biological child; however, this is not a practical definition that can be applied in a clinical setting to a patient’s diagnosis. Unlike infertility, sterility is rarely discussed in biomedical and clinical literature and is often used synonymously with infertility. Infertility affects about 10% of couples globally, but the prevalence of sterility remains unknown. We divide sterility into three subtypes natural, clinical, and hardship. To estimate sterility prevalence, we analyzed primary literature and meta-analysis papers on the rates of live births and pregnancies throughout several treatments of infertile couples (e.g., untreated patients, in vitro fertilization-treated, and patients administered other treatments). This analysis indicates that all treatments fail in delivering a biological child to most couples, suggesting that most infertile couples may fail to conceive. More comprehensive primary studies are needed to provide a precise estimate of sterility. Furthermore, research is needed to study the causes of sterility, as well as develop methods for diagnosis and treatment that are financially affordable and emotionally tolerable. Altogether, sterility is an under-discussed condition that is more common than expected, as many infertile couples are unable to conceive and are, in effect, sterile.

Male infertility is a growing global concern with increasing prevalence in both developing and developed nations. While many associations between environmental factors and male infertility have been explored, the relationship between sleep deprivation and male infertility remains underexplored. This narrative review examines the reported effects of sleep deprivation on the Hypothalamic––Gonadal (HPG) axis, Hypothalamic–Pituitary–Adrenal (HPA) axis, oxidative stress, and testicular function, and their consequential effects on male infertility. Disruption of the HPG axis results in altered follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels, leading to fluctuation in testosterone levels, negatively affecting spermatogenesis and other critical reproductive processes. Activation of the HPA axis, often due to stress, elevates cortisol levels, which, in turn, suppresses gonadotropin-releasing hormone (GnRH), impairing reproductive function. Reactive oxidative species (ROS) accumulate in periods of oxidative stress and have been shown to damage sperm and reduce their quality. The blood–testis barrier (BTB) is disrupted in states of sleep deprivation, leading to decreased sperm quality. A literature review was conducted using PubMed and Google Scholar to assess peer-reviewed studies from 1990 to 2024, revealing a complex interplay between sleep deprivation and male reproductive dysfunction. While existing studies support a link between sleep disturbances and hormonal dysregulation, further research is needed to establish causal relationships and identify potential therapeutic interventions. Addressing sleep deprivation may represent a modifiable factor in improving male fertility outcomes.

Fertility preservation technologies have existed for decades, and the field is rapidly advancing; limited data exist regarding the use of these technologies by transgender patients. Many options are available for transgender patients who wish to preserve fertility before transitioning. These options include the cryopreservation of gametes, embryos, or ovarian tissue. Currently, ejaculated, or testicular sperm, immature oocytes, and ovarian tissue can be preserved for later use, but no such use option exists for immature testicular tissue. Many financial, sociological, and legal barriers and a lack of awareness among physicians and patients also hinders the utilization of these fertility preservation services. While options are abundant, usage rates are relatively low. The initial data regarding the successful use of preserved tissues appears promising, with birth rates not dissimilar to non-transgender patients. Further investigations into this area are needed. In addition, counseling regarding fertility preservation options should become a significant part of the provider-patient conversation before transitioning therapies.

Fertility preservation technologies have existed for decades, and the field is rapidly advancing; limited data exist regarding the use of these technologies by transgender patients. Many options are available for transgender patients who wish to preserve fertility before transitioning. These options include the cryopreservation of gametes, ovarian tissue, or embryos. Currently, ejaculated, or testicular sperm, immature oocytes, and ovarian tissue can be preserved for later use, but no such use option exists for immature testicular tissue. Many financial, sociological, and legal barriers and a lack of awareness among physicians and patients also hindered the utilization of these fertility preservation services. While options are abundant, usage rates are relatively low. The initial data regarding the successful use of preserved tissues appears promising, with birth rates not dissimilar to non-transgender patients. Further investigations into this area are needed. In addition, counseling regarding fertility preservation options should become a significant part of the provider-patient conversation before transitioning therapies.; fertility; transgender; reproductive technology.

Male infertility is a growing global concern with increasing prevalence in both developing and developed nations. While many associations between environmental factors and male infertility have been explored, the relationship between sleep deprivation and male infertility remains underexplored. This narrative review examines the reported effects of sleep deprivation on the Hypothalamic-Pituitary-Gonadal (HPG) axis, Hypothalamic-Pituitary-Adrenal (HPA) axis, oxidative stress, and testicular function, and their consequential effects on male infertility. Disruption of the HPG axis results in altered FSH and LH levels, leading to fluctuation in testosterone levels, negatively affecting spermatogenesis and other critical reproductive processes. Activation of the HPA axis, often due to stress, elevates cortisol levels, which, in turn, suppresses gonadotropin-releasing hormone (GnRH), impairing reproductive function. Reactive oxidative species accumulate in periods of oxidative stress and have been shown to damage sperm and reduce their quality. The blood-testis-barrier (BTB) is disrupted in states of sleep deprivation, leading to decreased sperm quality. A literature review was conducted using PubMed and Google Scholar to assess peer-reviewed studies from 1990 to 2024, revealing a complex interplay between sleep deprivation and male reproductive dysfunction. While existing studies support a link between sleep disturbances and hormonal dysregulation, further research is needed to establish causal relationships and identify potential therapeutic interventions. Addressing sleep deprivation may represent a modifiable factor in improving male fertility outcomes.