Zoonotic diseases occur as a result of human interactions with animals with the inadvertent transmission of pathogens from one to another. Zoonoses remain a major cause of morbidity and mortality among human populations, as they have been a source of pandemics in human history. Viral zoonoses account for a significant percentage of pathogens of zoonotic sources, posing a huge risk to men’s general health and fertility. This review identifies the existing knowledge on the effects of viral zoonotic diseases on male fertility. Evidence from reviewed articles showed that viral zoonotic diseases elicit an immune reaction that induces inflammatory mediators and impairs testicular functions such as spermatogenesis and steroidogenesis, leading to abnormal semen parameters that lead to subfertility/infertility. Although most zoonotic viruses linger in semen long after recovery, their presence in semen does not directly translate to sexual transmission. There is a need to further delineate the possible risk of the sexual transmission of these diseases. While a few of the viral zoonotic diseases discussed have been well-studied, there is a need to place attention on others so as to fully understand their effects on male reproduction and therefore take the right steps towards preserving male fertility.

Bacterial zoonotic diseases hold significant public health importance due to their substantial contribution to human morbidity and mortality. These infections have been implicated in reducing the fertility rate among couples of reproductive age. Despite the increasing prevalence of infertility and sub-fertility in men, there has been limited investigation into the possible effects of bacterial zoonotic infections on the male reproductive system. The purpose of this review is to describe common bacterial zoonotic diseases and their effects on human reproduction in order to unveil the hidden roles these infections could play in male factor infertility. While there is a dearth of information on this subject from human studies, available evidence from experimental animals suggests that bacterial zoonotic diseases impair male reproductive functions and structures primarily through the activation of the inflammatory response and distortion of the antioxidant system, resulting in the generation of oxidative species. In light of the limited research on bacterial zoonotic diseases and their role in male reproduction, efforts must be directed towards the subject to unravel the underlying pathological mechanisms and reduce the incidence among the human populace, either through preventive or curative measures.

This review aims to bring attention to the growing issue of andropause, a condition that affects men as they age. The literature was identified by searching the major bibliographic databases, including PubMed, Google Scholar, EBSCOhost, Web of Science, and CINAHL. Studies were included if they focused on strategies for reducing and preventing andropause, published between 1980 and 2023. Andropause, which is often overlooked and misconceived, is the result of a decrease in testosterone production and can result in physical and psychological symptoms such as fatigue, weight gain, decreased libido, and depression. This paper reviews the literature on the prevalence, detection, and management of andropause. It is important for the medical community to recognize andropause, as diagnosing and treating the condition can significantly improve the quality of life. The review canvases several studies to understand andropause comprehensively, highlighting various biomarkers and diagnostic criteria, possible therapies, and potential risks and complications associated with the condition. In addition, this review offers practical suggestions to health professionals, helping them recognize patients at risk of andropause, assess patients for the condition, and provide appropriate treatments. Furthermore, it emphasizes the importance of regular screening and active monitoring for any possible early warning signs of andropause. This review provides a comprehensive overview of andropause, from identification to management. It demonstrates the need for increased awareness and acknowledgment of andropause among medical professionals in order to ensure that all men get the support they need throughout the aging process.

Polycystic ovary syndrome (PCOS) intersects with substance use through specific biological pathways, as demonstrated by this systematic review of 87 peer-reviewed studies from 2014 to 2024. The analysis reveals three clinically significant mechanisms: chronic alcohol consumption (> 3 drinks/day) elevates serum testosterone through dual pathways—reducing hepatic SHBG production by 40–60% while directly stimulating ovarian theca cell androgen synthesis via oxidative stress. Nicotine exposure differentially impacts PCOS phenotypes, exacerbating adrenal hyperandrogenism in obese patients through nAChRα7-mediated 17α-hydroxylase upregulation while showing minimal metabolic effects in lean individuals. Cannabis use alters reproductive neuroendocrinology, with weekly consumption correlating to prolonged follicular phases and reduced ovulation rates through CB1 receptor-mediated suppression of LH surge amplitude. These substance-specific interactions compound core PCOS pathophysiology. Alcohol’s hepatic effects amplify existing hyperandrogenemia, nicotine’s adrenal stimulation creates an additional androgen source beyond ovarian dysfunction, and cannabis-induced gonadotropin disruption exacerbates anovulation. Clinically, the findings necessitate routine substance use screening in PCOS management and phenotype-specific interventions—particularly adrenal-focused approaches for nicotine users and GnRH pulse stabilization for cannabis consumers. The review identifies critical research gaps, including dose–response thresholds for substance effects and demographic disparities in study populations. Future investigations should prioritize longitudinal designs to establish temporal relationships and controlled interventions targeting identified mechanisms. These evidence-based insights refine clinical understanding of how specific substances modify PCOS trajectories, moving beyond generalized associations to delineate actionable biological pathways for therapeutic targeting.