Background/Objectives: Benign prostatic hyperplasia (BPH) is among the most common conditions affecting men as they age, resulting in lower urinary tract symptoms (LUTS) that can profoundly impact quality of life. While historically attributed primarily to androgenic imbalances, current evidence implicates additional factors—particularly oxidative stress (OS) and chronic inflammation—in BPH pathogenesis. This review aims to synthesize research on the interplay between OS, inflammation, and hormonal regulation in BPH, emphasizing their clinical relevance and potential therapeutic implications. Methods: A comprehensive review of peer-reviewed literature was conducted focusing on mechanistic studies, clinical trials, and observational reports. Searches included data on ROS generation, antioxidant capacity, inflammatory mediators, and their contribution to pathological prostatic overgrowth. Potential interventions targeting OS—such as antioxidant supplementation, anti-inflammatory drugs, vitamin D receptor agonists, and phytotherapeutics—were also evaluated for their efficacy and safety profiles. Results: Chronic inflammation and OS were consistently identified within hyperplastic prostate tissue. Excessive ROS production, diminished antioxidant defense, and sustained cytokine release create a proproliferative and antiapoptotic environment, accelerating disease progression. Metabolic comorbidities (e.g., obesity, insulin resistance) further exacerbate these imbalances. Standard therapies (α-blockers and 5-ARIs) effectively relieve symptoms but do not directly address the oxidative–inflammatory axis. Emerging evidence suggests that pharmacological and dietary approaches targeting OS and inflammation may reduce prostate volume expansion and alleviate LUTS. Conclusions: Findings indicate that OS and inflammation are key contributors to BPH progression. Incorporating antioxidant and anti-inflammatory strategies alongside conventional treatments holds promise for improving clinical outcomes and patient quality of life. Future research should focus on validating OS-specific biomarkers and optimizing personalized therapy regimens.

Male infertility is an under-recognized global health burden. Accumulating evidence position the intestinal microbiota as a pivotal regulator of testicular function, underpinning the emerging gut microbiota–testis axis. This narrative review introduces the conceptual term “androbactome”, referring to gut microorganisms and microbial genes that are hypothesized to influence androgen biosynthesis, spermatogenesis, and broader reproductive endocrinology. The documented worldwide decline in sperm concentration heightens the urgency of clarifying microbe-mediated influences on male reproductive capacity. The synthesis of preclinical and clinical findings reveals four principal pathways by which dysbiosis compromises fertility: systemic inflammation, oxidative stress, endocrine disruption, and epigenetic alteration. Lipopolysaccharide-driven cytokinaemia, reactive oxygen species generation, hypothalamic–pituitary–gonadal axis suppression, and aberrant germ cell methylation collectively impair sperm quality and hormonal balance. Short-chain fatty acids, secondary bile acids, and indole derivatives emerge as pivotal messengers within this crosstalk. Therapeutic approaches targeting the androbactome, namely dietary optimization, probiotic or prebiotic supplementation, and fecal microbiota transplantation, have demonstrated encouraging improvements in sperm parameters and testosterone levels, yet the causal inference is constrained by predominantly cross-sectional designs and limited long-term safety data. Recognizing the androbactome as a modifiable determinant of male fertility may open new avenues for personalized diagnosis, risk stratification, and adjunctive therapy in regard to idiopathic infertility. The integration of multi-omics platforms to characterize microbial and metabolomic signatures promises to enrich diagnostic algorithms and guide precision interventions, but rigorously controlled longitudinal and interventional studies are required to secure a translational impact.

Male infertility is a prevalent condition affecting approximately 15% of couples worldwide. Recent evidence indicates that, beyond its immediate reproductive implications, male infertility may reflect broader health concerns. Large-scale cohort studies consistently show that men with poorer semen parameters have elevated all-cause mortality compared to fertile counterparts, with a dose-dependent pattern whereby more severe abnormalities correlate with a higher risk of early death. Proposed mechanisms linking infertility to reduced life expectancy encompass genetic, hormonal, and lifestyle factors. For instance, Klinefelter syndrome exemplifies a genetic cause of azoospermia that also predisposes to metabolic syndrome, diabetes, and certain malignancies. Low testosterone, a frequent finding in testicular dysfunction, is implicated in obesity, insulin resistance, and cardiovascular disease, all of which can shorten lifespan. Additionally, psychosocial stress and depression—commonly reported among infertile men—may contribute to health-compromising behaviors. Environmental exposures and socioeconomic factors further compound these risks. Collectively, these data underscore the importance of recognizing male infertility as an early indicator of potentially modifiable health vulnerabilities. A comprehensive evaluation of infertile men should therefore extend beyond fertility assessments to include screening for chronic diseases, hormonal imbalances, and mental health issues. Targeted surveillance for specific cancers (e.g., testicular and prostate) and early interventions—such as lifestyle modifications, appropriate hormonal therapies, and psychosocial support—can improve both reproductive outcomes and long-term well-being. Given these insights, male fertility assessment may serve as a valuable gateway to broader men’s healthcare, prompting proactive strategies that mitigate associated risks and potentially enhance longevity.

Introduction: Multiple Sclerosis (MS) is a degenerative neurological disease that usually occurs between the ages of 20 and 50 years. Sexuality issues are important factors that affect the quality of life of patients.Aim: To determine and evaluate the prevalence of female sexual dysfunction (FSD) in Greek women with MS and correlate it with organic and psychological factors.Methods: 248 consecutive women with MS, aged over 18 who admitted to our outpatient clinics from February 2016 to March 2017 were included in the study. Demographics (age, marital status, menopause status, number of children) and disease-related data such as the duration of the disease, Expanded Disability Status Scale (EDSS) and medication for MS obtained.Main Outcome Measure: All participants completed the Greek validated versions of the Depression, Anxiety, Stress Scale (DASS-21) and the Female Sexual Function Inventory (FSFI) questionnaires. Statistics used to estimate the prevalence of FSD and its correlation with organic (age, EDSS, duration of the disease, menopause status) and psychological factors (depression, anxiety, stress).Results: FSD was diagnosed in 64.5% of our sample. Age was associated with most subscales of the FSFI. There was no significant correlation in FSFI subscales with the disease duration. Correlation of EDSS and FSFI scores was found to be statistically significant with a negative correlation in all subscales apart from the Satisfaction subscale. Regarding the association between DASS domains and FSFI subscales, there were no significant correlations.Conclusion: FSD is common among Greek women; it is influenced by age, severity of disease, and it is independent of the existence of depression, anxiety, and stress.

Background/Objectives: Non-obstructive azoospermia (NOA) is a severe form of male infertility characterized by the absence of sperm in the ejaculate due to impaired spermatogenesis. Testicular sperm extraction (TESE) combined with intracytoplasmic sperm injection is the primary treatment, but success rates are unpredictable, causing significant emotional and financial burdens. Traditional clinical and hormonal predictors have shown inconsistent reliability. This review aims to evaluate current and emerging non-invasive preoperative predictors of successful sperm retrieval in men with NOA, highlighting promising biomarkers and their potential clinical applications. Methods: A comprehensive literature review was conducted, examining studies on clinical and hormonal factors, imaging techniques, molecular biology biomarkers, and genetic testing related to TESE outcomes in NOA patients. The potential role of artificial intelligence and machine learning in enhancing predictive models was also explored. Results: Traditional predictors such as patient age, body mass index, infertility duration, testicular volume, and serum hormone levels (follicle-stimulating hormone, luteinizing hormone, inhibin B) have limited predictive value for TESE success. Emerging non-invasive biomarkers—including anti-Müllerian hormone levels, inhibin B to anti-Müllerian hormone ratio, specific microRNAs, long non-coding RNAs, circular RNAs, and germ-cell-specific proteins like TEX101—show promise in predicting successful sperm retrieval. Advanced imaging techniques like high-frequency ultrasound and functional magnetic resonance imaging offer potential but require further validation. Integrating molecular biomarkers with artificial intelligence and machine learning algorithms may enhance predictive accuracy. Conclusions: Predicting TESE outcomes in men with NOA remains challenging using conventional clinical and hormonal parameters. Emerging non-invasive biomarkers offer significant potential to improve predictive models but require validation through large-scale studies. Incorporating artificial intelligence and machine learning could further refine predictive accuracy, aiding clinical decision-making and improving patient counseling and treatment strategies in NOA.

Background/Objectives: Varicoceles are a common contributor to male infertility, significantly impacting male-factor infertility cases. Traditional diagnostic methods often lack the sensitivity to detect the molecular and cellular disruptions caused by varicoceles, limiting the development of effective, personalized treatments. This narrative review aims to explore the advancements in proteomics and metabolomics as innovative, non-invasive diagnostic tools for varicocele-associated male infertility and their potential in guiding personalized therapeutic strategies. Methods: A comprehensive literature search was conducted using databases such as PubMed, Scopus, and Web of Science up to October 2024. Studies focusing on the application of proteomic and metabolomic analyses in varicocele-associated male infertility were selected. The findings were critically analyzed to synthesize current knowledge and identify future research directions. Results: Proteomic analyses revealed differentially expressed proteins in the sperm and seminal plasma of varicocele patients, revealing disruptions in pathways related to oxidative stress, mitochondrial dysfunction, apoptosis, and energy metabolism. Key proteins such as heat shock proteins, mitochondrial enzymes, and apoptotic regulators were notably altered. Metabolomic profiling uncovered specific metabolites in seminal plasma—such as decreased levels of lysine, valine, and fructose—that correlate with impaired sperm function and fertility potential. The integration of proteomic and metabolomic data provides a comprehensive molecular fingerprint of varicocele-induced infertility, facilitating the identification of novel biomarkers for early diagnosis and the development of personalized therapeutic interventions. Conclusions: Advances in proteomics and metabolomics have significantly enhanced our understanding of the molecular mechanisms underlying varicocele-associated male infertility. These “omics” technologies hold great promise for improving diagnostic accuracy and personalizing treatment, ultimately leading to better outcomes for affected men. Future large-scale clinical trials and validations are essential to confirm these biomarkers and facilitate their integration into routine clinical practice.