Impact of Psychostimulant Exposure on Male Fertility and Spermatogenic Function

This review synthesizes current experimental and clinical evidence regarding the effects of psychostimulants, including cocaine, methamphetamine, methylphenidate, nicotine, and caffeine, on male reproductive function. The primary focus is on the mechanisms by which these substances disrupt spermatogenesis via hormonal, cellular, oxidative, and epigenetic pathways.

A narrative synthesis of recent literature was conducted, integrating findings from animal models, human observational studies, imaging data, and mechanistic research. The review incorporates studies assessing endocrine parameters, testicular histology, sperm quality, oxidative stress markers, and emerging epigenetic profiles.

Psychostimulants consistently disrupt the hypothalamic-pituitary-gonadal axis, lower testosterone levels, and compromise the function of both Leydig and Sertoli cells. Animal models develop seminiferous tubule atrophy, mitochondrial dysfunction, increased reactive oxygen species, and disruption of the blood-testis barrier. Human neuroimaging and post-mortem findings support testicular size reduction and abnormal architecture. Sperm analyses show decreased concentration and motility, abnormal morphology, enhanced DNA fragmentation, and reduced mitochondrial activity. Co-exposures-alcohol, cannabis, and antidepressants-add stress and adolescent use, further increasing toxicity. There is emerging evidence of persistent epigenetic changes, with possible transgenerational effects.

Available data support the fact that therapeutic abuse or recreational use of psychostimulants may severely impair male fertility through endocrine disruption, oxidative stress, testicular degeneration, and epigenetic changes. In light of increasing worldwide consumption among reproductive-age men, appropriate counseling, hormonal, and semen monitoring, as well as prevention measures, are urgently required. Further research should establish dose thresholds, reversibility of the effects, and, finally, long-term reproductive consequences.