Psychological Stress and Male Fertility: Pathophysiological Mechanisms, Experimental Models, and Therapeutic Approaches—A Narrative Review
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Objective: This narrative review aimed to synthesize current evidence regarding the biological mechanisms linking psychological stress with male reproductive dysfunction and to evaluate potential therapeutic strategies targeting stress-related fertility impairment.
Methods and Materials: A structured narrative review was conducted using PubMed, Scopus, and ScienceDirect databases. Studies published between 1997 and 2024 were identified using keywords related to psychological stress, male fertility, cortisol, hypothalamic–pituitary–adrenal (HPA) axis, hypothalamic–pituitary–gonadal (HPG) axis, oxidative stress, inflammation, spermatogenesis, and semen quality. Human studies, animal models, and experimental investigations examining stress-related reproductive alterations were included. Findings were synthesized narratively according to neuroendocrine mechanisms, oxidative and inflammatory pathways, experimental models, and therapeutic approaches.
Findings: Current evidence suggests that chronic psychological stress may influence male reproductive function through interacting pathways involving HPA axis activation, cortisol elevation, HPG axis suppression, oxidative stress, inflammation, and behavioral factors. Experimental studies demonstrate that increased reactive oxygen species, inflammatory cytokines, and altered hormonal regulation may contribute to impaired spermatogenesis, sperm DNA damage, and reduced semen quality. Animal models provide important mechanistic insights; however, their translation to humans remains limited. Therapeutic approaches, including cognitive-behavioral interventions, lifestyle modification, antioxidant strategies, and selected phytotherapeutic agents, show potential benefits, although clinical evidence remains heterogeneous.
Conclusion: Psychological stress may contribute to male reproductive dysfunction through complex neuroendocrine, oxidative, inflammatory, and behavioral mechanisms. However, current human evidence is insufficient to establish definitive causality. Longitudinal studies and controlled clinical trials are required to clarify mechanisms and evaluate targeted interventions.
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