Abstract

Progressive deterioration of male reproductive function is occurring in Western countries. Environmental factors and unhealthy lifestyles have been implicated in the decline of testosterone levels and sperm production observed in the last fifty years. Among unhealthy lifestyles, substance and drug abuse is a recognized cause of possible alterations of steroidogenesis and spermatogenesis. Alcohol, opioids and anabolic-androgenic steroids are capable to reduce testosterone production in male interfering with testicular and/or hypothalamic-pituitary function. Other substances such as nicotine, cannabis, and amphetamines alter spermatogenesis inducing oxidative stress and subsequent apoptosis in testicular tissue. Substance and drug abuse is a potentially reversible cause of hypogonadism, defined as the failure of the testis to produce physiological concentrations of testosterone and/or a normal number of spermatozoa. The identification of the abuse is important because the withdrawal of substance intake can reverse the clinical syndrome. This review summarizes the most important clinical and experimental evidence on the effect of substance abuse on testosterone and sperm production.

Highlights

  • According to the most recent definition, hypogonadism is a clinical syndrome resulting from the failure of the testis to produce physiological concentrations of testosterone and/or a normal number of spermatozoa due to pathologies of the hypothalamic–pituitary–testicular axis [1].Pathogenic noxae acting at testicular level give rise to a syndrome characterized by low testosterone concentrations, impairment of spermatogenesis, and elevated gonadotropin levels, defined as primary hypogonadism

  • In conditions when SHGB levels are reduced, total testosterone concentrations could be below normal values even if free testosterone levels are in the normal range

  • Since testes are sensitive to temperature and HSP are produced in response to thermic stress to stop caspase activation and inhibit the apoptotic process, the Authors hypothesized that MDMA-induced hyperthermia could activate apoptosis in rat testicular tissue [119]

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Summary

Introduction

According to the most recent definition, hypogonadism is a clinical syndrome resulting from the failure of the testis to produce physiological concentrations of testosterone and/or a normal number of spermatozoa due to pathologies of the hypothalamic–pituitary–testicular axis [1]. Secondary hypogonadism is caused by a dysfunction of the hypothalamus–pituitary unit, resulting in low testosterone concentrations, impairment of spermatogenesis, and low or inappropriately normal gonadotropin levels [1]. In conditions when SHGB levels are reduced (e.g., obesity, type 2 diabetes mellitus, androgen use), total testosterone concentrations could be below normal values even if free testosterone levels are in the normal range. Most laboratories use immunoassays that are less accurate In this case, to calculate free testosterone starting from total testosterone, SHBG, and albumin values is preferable [1]. Alcohol abuse, cigarette smoking, excessive caffeine intake, illicit drug intake, opioid consumption, and inappropriate use of anabolic steroids have been studied as a possible cause of reduced sperm production and/or reduced testosterone levels in hypogonadal men [6]. Data obtained in animals are not always reproducible in humans; so some aspects regarding the mechanisms of action of several substances on the reproductive function must be further clarified

Alcohol
Effects on Testosterone Production
Effects on Spermatogenesis
Cigarette Smoking
Caffeine
Cannabis
Cocaine
Opioids
Anabolic-Androgenic Steroids
Findings
10. Conclusions
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