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Infections and Male Infertility (Part I): General Pathophysiology, Diagnosis, and Treatment explores the complex link between infections and male infertility, providing a comprehensive examination of their impact on reproductive health. This book integrates key concepts from molecular biology, immunology, and clinical practice to highlight the pathophysiology, diagnosis, and treatment of infection-induced infertility.
Key Features:
- Multidisciplinary insights from molecular biology, immunology, and reproductive medicine.
- Comprehensive coverage of infections affecting male fertility, including diagnosis and treatment.
- Discussion of emerging therapies, including stem cell research and personalized medicine.
Readership:
This book is an essential resource for medical professionals, researchers, and students in reproductive medicine, urology, and andrology. It is particularly valuable for clinicians, scientists, and healthcare policymakers involved in male infertility and reproductive health
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Seitenzahl: 405
Veröffentlichungsjahr: 2025
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The realm of medical science is both vast and perpetually developing, embodying a myriad of interconnected specialties, each illuminating distinct aspects of truth while also preserving their own unresolved mysteries. Various subfields of male infertility, previously obscured by bias and misconceptions, have now emerged as topics of high research interest. The importance of understanding the underlying mechanisms of male infertility is being increasingly acknowledged, yet certain gaps in knowledge persist, particularly in understanding the intricate role that infections play in male infertility. ‘Infections and Male Infertility: Part I: General Pathophysiology, Diagnosis, and Treatment’, penned by Dr. Sulagna Dutta and Dr. Pallav Sengupta, serves as an enlightening exploration into this multifaceted domain.
This pivotal composition amalgamates sound scientific research with clinical insight to unravel the complex association between infections and male infertility. By employing this method, Drs. Dutta and Sengupta shed light on the influence of infections on the pathophysiology of male infertility, a subject that is often neglected but critical to a comprehensive grasp of the field. It possesses the potential to reshape our viewpoints and, possibly, our medical practices.
The authors' extensive expertise and experience resonate throughout the text, emphasizing the significance of their contributions. Their committed review of the current literature and original research helps bridge a crucial gap in the field. The organization of the book—initiating with an exhaustive investigation into the general pathophysiology of male infertility, transitioning into the role of infections, and concluding with the diagnosis and treatment of these conditions—provides a graduated learning journey that is both intellectually invigorating and pragmatically applicable.
The true value of this work goes beyond mere academic rigor. By focusing on infection-induced male infertility, an area often fraught with misunderstanding and insufficient research, Drs. Dutta and Sengupta present comprehensive views on male fertility. Through an exhaustive discussion, they delve into various aspects of infection conditions, inflammatory processes, and the complex interactions between infection, inflammation, endocrine systems, and reproduction. Their insights not only enable more nuanced conversations and interventions but also pave the way for the scientific community, researchers, students, and general readers who are more informed on these critical subjects.
‘Infections and Male Infertility: Part I: General Pathophysiology, Diagnosis and Treatment’ functions not only as a rich repository of scientific data but also as a reflection of the progressive evolution of our shared understanding of reproductive health. It embodies the scientific and societal obligation to dissect intricate interactions and to perpetually seek a more refined comprehension of human reproductive immunology.
Whether you are an established medical professional, a researcher, a novice embarking on your academic journey in reproductive medicine, or an inquisitive reader, this publication promises to inform, question, and inspire.
As we immerse ourselves in this text, let us recollect the statement by William Osler, ‘Medicine is a science of uncertainty and an art of probability.’ Here's to the anticipation of scientific discoveries and the skillful practice of medicine, as steered by the trailblazing work of Dr. Sulagna Dutta and Dr. Pallav Sengupta.
The intricate subject of male infertility has, for an extended period, engaged the attention of the medical community in a mix of intrigue and difficulty. With immense excitement, we present our work titled ‘Infections and Male Infertility: Part I: General Pathophysiology, Diagnosis, and Treatment’, which is a thorough investigation into one of the frequently underappreciated origins of male infertility.
The intent of this book is to provide an all-encompassing examination of the complex correlation between infectious diseases and male infertility. Our goal is to deliver a lucid narrative that transitions from the molecular interactions at the level of pathophysiology to the broader clinical outcomes of these interactions.
Drawing upon a broad spectrum of scientific inquiry, our book delves into the underlying mechanisms through which a variety of infections may perturb the male reproductive system. The biochemical pathways, immunological reactions, and genetic modifications that participate in this process are meticulously elaborated upon to elucidate this complex issue. The book endeavors to establish a theoretical and practical link between the origins of infections and their clinical implications for male fertility.
We hold the conviction that a precise diagnosis is the cornerstone of effective therapeutic intervention. In line with this, our text outlines numerous diagnostic methodologies, their deployment, and interpretation within the context of infections inducing male infertility. By clarifying these techniques, we aim to empower clinicians to better recognize and comprehend the etiology of male infertility.
The concluding segment centers on the most recent therapeutic strategies. We illuminate the contemporary cutting-edge treatments, their advantages, and restrictions while accentuating potential directions for forthcoming interventions. The book particularly emphasizes the need for a tailored, patient-centric approach to managing this condition.
This publication serves a two-fold purpose: It offers an advanced reference for medical professionals, equipping them with a deeper insight into the sophisticated interaction between infections and male infertility. Concurrently, it offers a roadmap for researchers, laying the groundwork for future investigations into the pathophysiology, diagnosis, and treatment of infections leading to male infertility.
The process of creating this book proved to be both demanding and fulfilling. We express our gratitude to the many researchers and clinicians whose invaluable contributions have set the stage for this exhaustive analysis. With the publication of this work, we aspire to ignite further research and discussion, thereby paving the way to enhanced diagnostic and therapeutic strategies for male infertility.
We appreciate your companionship in this exploration of a relatively uncharted facet of reproductive medicine. We trust that ‘Infections and Male Infertility: Part I: General Pathophysiology, Diagnosis, and Treatment’ will amplify your comprehension of this intricate domain and encourage ongoing research, innovation, and improvement in patient care.
Male infertility, defined as the inability to achieve conception after a year of unprotected intercourse, is an imperative global issue. Understanding its etiology is vital for effective diagnosis, treatment, and support. The chapter provides a comprehensive overview of the anatomy and physiology of the male reproductive system, addressing the causes of male infertility. It begins by introducing male infertility and stressing the importance of investigating its causes. An extensive examination of the male reproductive system follows, encompassing structural attributes, functionalities, and endocrine regulation. The chapter identifies genetic factors, environmental exposures, lifestyle choices, and pathological conditions as critical contributors to male infertility. Additionally, it explores the psychological toll of infertility, highlighting emotional distress and coping strategies while emphasizing the importance of professional and social support. The chapter concludes by discussing innovative research and treatment avenues, including genomics, epigenomics, proteomics, metabolomics, and spermatogonial stem cell therapy as promising fields. The roles of assisted reproductive technologies, male contraception, and lifestyle and environmental factors are also evaluated. This chapter underscores male infertility as a complex issue with a heterogeneous etiology and aims to foster an in-depth understanding and improve reproductive health outcomes for affected individuals and couples.
Infertility, a term that bears emotional connotations for many, is a common medical issue affecting approximately 15% of couples worldwide. Among these, nearly half can be attributed to male infertility [1]. Male infertility, in the simplest terms, is defined as the inability of a man to cause pregnancy in a fertile female after a year of unprotected intercourse [2]. It has myriad causes that span from physical and psychological to genetic and environmental. As our understanding of these factors continues to deepen, we hope to improve not only the diagnosis but also the treatment options available to affected individuals.
The importance and prevalence of male infertility are often underestimated in societal discussions around fertility, which typically focus more on women. However, this issue holds substantial weight as it affects a significant proportion of men globally. The World Health Organization estimates that up to 7% of men worldwide are affected by some form of infertility [3]. This percentage, though seemingly small, translates into millions of individuals and couples grappling with the often-devastating news of fertility issues. Furthermore, the male factor contributes to around 50% of all cases of infertility in couples, emphasizing the gender parity in this issue [4].
The rationale for the present chapter is multifaceted. Firstly, it aims to offer a comprehensive overview of male infertility and its causes to facilitate a broader understanding of the topic. As this is a problem with numerous contributing factors, an in-depth exploration of each cause is essential to fully grasp the complexity of male infertility. Secondly, it underscores the significance and prevalence of male infertility, attempting to recalibrate the often female-focused narrative around infertility. Finally, it hopes to provide a foundation of knowledge from which further research and treatment options can be developed, potentially benefiting millions of individuals worldwide.
In the forthcoming sections, we will delve into the biological mechanics of male infertility, outline the most common causes, and discuss the latest research findings in the field. The chapter will also shed light on the physiological, genetic, and environmental contributors to male infertility and review the existing diagnostic techniques and therapeutic interventions. By enhancing our understanding of this critical issue, we hope to contribute to the ongoing efforts to develop better strategies for diagnosis, management, and treatment of male infertility.
Male infertility is defined as the inability of a man to impregnate a fertile female partner despite regular, unprotected sexual intercourse for a year or longer [5]. This can occur due to several factors, including low sperm count, poor sperm motility, abnormal sperm morphology, or a blockage in the reproductive tract. Other possible causes of male infertility include hormonal imbalances, genetic abnormalities, and certain medical conditions such as diabetes or a history of chemotherapy [6].
Understanding male infertility is essential for several reasons. First, male infertility is a widespread issue that can significantly impact the ability of a couple to conceive. Approximately 30% of infertility cases are due to male factors alone, and another 20-30% are caused by both male and female factors [4]. This highlights the need for increased awareness and understanding of male infertility, as it plays a significant role in infertility cases. Second, understanding male infertility can help identify potential causes and treatments. For example, low sperm count can be caused by a variety of factors, including lifestyle choices such as smoking, excessive alcohol consumption, and a sedentary lifestyle [7]. Identifying and addressing these factors can potentially improve the fertility of a man. Additionally, certain medical conditions or genetic abnormalities may require more advanced treatment options, such as assisted reproductive technologies (ART) [8]. Third, understanding male infertility can help alleviate the stigma surrounding infertility. Infertility can be a sensitive topic, and many men may feel ashamed or embarrassed to seek help. However, understanding that male infertility is a medical condition that affects many men can help reduce this stigma and encourage men to seek the necessary medical care.
The male reproductive system is made up of several organs, which are responsible for producing and transporting sperm. The primary organs of the male reproductive system include the testes, epididymis, vas deferens, seminal vesicles, prostate gland, and urethra Fig. (1).
The testes are the primary male reproductive organs. They are responsible for producing sperm and the hormone testosterone. The testes are located in the scrotum, which is a pouch of skin that hangs below the penis. The testes are composed of numerous small, coiled tubules called seminiferous tubules, which produce sperm [9]. The Leydig cells of the testes produce testosterone [10].
The epididymis is a long, coiled tube located behind each testicle. It is responsible for storing sperm that have been produced in the testes until they are ready to be ejaculated. During this time, the sperm mature and gain the ability to swim [11].
The vas deferens is a muscular tube that transports mature sperm from the epididymis to the urethra. It travels from the epididymis through the inguinal canal and into the abdomen, where it passes over the bladder and joins the seminal vesicles to form the ejaculatory duct [9, 12].
The seminal vesicles are a pair of glands located at the base of the bladder. They secrete a fluid that makes up the majority of the volume of semen. The fluid contains fructose, which provides energy for the sperm, and other nutrients [13].
Fig. (1)) Anatomy of the male reproductive system (A) indicating the organs included. (B) The primary function of the testis is to produce spermatozoa by the process of spermatogenesis, followed by sperm cell maturation in the epididymis, resulting in the development of mature spermatozoa (C).The prostate gland is a walnut-sized gland located beneath the bladder. It surrounds the urethra, which is the tube that carries urine and semen out of the body [9]. The prostate gland secretes a fluid that helps to nourish and protect the sperm. It also helps to make the semen more alkaline, which protects the sperm from the acidic environment of the vagina [14].
The urethra is the tube that carries urine and semen out of the body. It passes through the prostate gland and the penis. During ejaculation, the urethra carries the semen out of the male reproductive tract [15].
The male reproductive system is a complex assembly of organs and structures, including the testes, epididymis, vas deferens, seminal vesicles, prostate gland, and penis. Its primary function is the production and delivery of sperm, the male reproductive cell, into the female reproductive tract for fertilization [16].
Spermatogenesis is the process of sperm cell production that occurs in the seminiferous tubules of the testes. It begins during puberty and continues throughout the life of a man. The process consists of three main phases: mitosis, meiosis, and spermiogenesis. In the mitotic phase, spermatogonial stem cells (SSCs), which are located in the basal compartment of the seminiferous tubules, undergo mitosis to produce two types of daughter cells: more SSCs (to maintain the stem cell pool) and primary spermatocytes [17]. This phase ensures a continuous supply of cells for spermatogenesis. During the meiotic phase, primary spermatocytes undergo meiosis I and II to form secondary spermatocytes and, subsequently, spermatids. Meiosis I, a reductional division, reduces the chromosome number from 46 (diploid) to 23 (haploid). Meiosis II, an equational division, does not alter the chromosome number but separates the sister chromatids. The end products of these two rounds of divisions are haploid spermatids [17].
Spermiogenesis is the transformation of haploid spermatids into mature spermatozoa. It involves several morphological changes that include the formation of the acrosome (a specialized structure that contains enzymes crucial for fertilization), elongation and compaction of the nucleus, formation of the flagellum (tail), and removal of unnecessary cytoplasm. The end result is a motile sperm cell specialized for the delivery of the male genome to the egg [17, 18].
Sperm maturation or capacitation refers to a complex biochemical process that enables sperm cells to become competent to fertilize an egg. This process involves a series of physiological changes that occur in the sperm cells as they move through the male reproductive tract, including the epididymis, vas deferens, and seminal vesicles [11, 13]. Sperm maturation or capacitation is a process that prepares sperm cells for fertilization [19]. This process involves several steps, including changes in the sperm cell membrane, the cytoskeleton, and the acrosome. The process of sperm maturation can be divided into two stages: the first stage is known as the ‘pre-capacitation’ stage, and the second stage is known as the ‘capacitation’ stage [19].
The pre-capacitation stage is the first step in the process of sperm maturation. During this stage, the sperm cells undergo several changes that make them competent to move through the female reproductive tract. One of the significant changes that occur during this stage is the loss of cholesterol from the sperm cell membrane [20]. This loss of cholesterol leads to an increase in the fluidity of the membrane, which is essential for the sperm cells to move through the female reproductive tract. Another significant change that occurs during this stage is the reorganization of the cytoskeleton. The cytoskeleton is a network of protein fibers that gives the cell its shape and structure. During the pre-capacitation stage, the cytoskeleton undergoes a reorganization that enables the sperm cells to move more efficiently [21]. This reorganization also results in the development of the flagellum, which is the tail-like structure that enables the sperm cells to move [21, 22].
The second stage of sperm maturation is known as the capacitation stage. During this stage, the sperm cells undergo several changes that make them competent to fertilize an egg. One of the significant changes that occur during this stage is the activation of the cAMP-dependent protein kinase A (PKA) pathway [23]. This pathway is responsible for the phosphorylation of proteins that are involved in sperm motility, capacitation, and acrosome reaction. Another significant change that occurs during this stage is the activation of the protein tyrosine kinase (PTK) pathway. This pathway is responsible for the phosphorylation of proteins that are involved in sperm-egg binding, acrosome reaction, and zona pellucida penetration [24]. The activation of the PTK pathway also results in the release of the hyaluronidase enzyme, which is involved in breaking down the hyaluronic acid in the cumulus oophorus that surrounds the egg [23, 24].
Sperm maturation or capacitation is a crucial process for male fertility. It is essential for the sperm cells to become competent to fertilize an egg [19, 22]. Without this process, the sperm cells would not be able to move through the female reproductive tract, bind to the egg, and fertilize it. Several factors can affect the process of sperm maturation or capacitation, including environmental factors, hormonal imbalances, and genetic abnormalities [22]. These factors can lead to a decrease in male fertility and can cause infertility.
After formation, spermatozoa are transported from the seminiferous tubules to the epididymis, a convoluted tube that provides a suitable environment for sperm maturation and storage. During their transit through the epididymis, sperm acquire their motility and the ability to fertilize an egg [11]. Sperm can be stored in the epididymis for several weeks. Upon sexual arousal, mature sperm are transported from the epididymis through the vas deferens, which carries sperm to the ejaculatory duct. During ejaculation, sperm is mixed with seminal fluid from the seminal vesicles, prostate gland, and bulbourethral glands to form semen. The semen is then propelled through the urethra and out of the penis [21].
Testosterone, the primary male sex hormone, is synthesized in the Leydig cells of the testes through a process known as steroidogenesis [25]. The process begins with the conversion of cholesterol to pregnenoloneviathe enzymatic action of P450scc. Pregnenolone is then converted to progesterone, which is subsequently transformed into androstenedione through several enzymatic steps. Androstenedione is finally converted to testosterone by the enzyme 17β-hydroxysteroid dehydrogenase. Testosterone plays a crucial role in the male reproductive system, which is described in detail in the forthcoming sections [26].
Each of these stages involves finely tuned, complex biological mechanisms regulated by a wide array of hormones and cellular signals, ensuring the continuous production, maturation, and delivery of healthy sperm cells, thereby maintaining male fertility [21]. The role of testosterone, produced by the process of steroidogenesis, underscores its importance in both initiating and maintaining these processes [10]. From the initiation of spermatogenesis in the seminiferous tubules to the storage and transport of mature sperm in the epididymis and vas deferens, every aspect of this journey is crucial for successful fertilization [17]. The production of seminal fluid by the seminal vesicles, prostate gland, and bulbourethral glands further supports the function of the mature sperm, aiding their survival and successful journey to the egg [9]. With each stage taking place in different parts of the male reproductive system, this system showcases an intricate and dynamic interaction of structure and function, underlying the propagation of life. Each step is a critical piece in the complex puzzle of human reproduction, providing profound insights into the marvels of biological design and function.
Thus, the male reproductive system is a marvel of biological engineering that performs its functions with extraordinary precision. It is an intricate network of processes that ensure the perpetuation of genetic material, thereby playing a pivotal role in the preservation of human life. From spermatogenesis and spermiogenesis to sperm transport, storage, and steroidogenesis, every function has a crucial role to play, highlighting the remarkable complexity and precision of the male reproductive system.
Hormones are the key regulators of the male reproductive system, as they govern the development and function of the testes, the accessory glands, and the external genitalia. The endocrine system, which consists of various glands that secrete hormones, controls the hormonal regulation of the male reproductive system. The hypothalamus, pituitary gland, and testes are the major components involved in this process Fig. (2).
Fig. (2)) Hormonal regulations of male reproductive functions.As discussed earlier, the testes are the primary male reproductive organs, and they are responsible for the production of testosterone, the primary male sex hormone [9]. Testosterone is secreted by the Leydig cells of the testes, and its secretion is regulated by LH secreted by the pituitary gland. LH stimulates the Leydig cells to produce testosterone, which then acts on the seminiferous tubules to regulate spermatogenesis, the process of sperm production [16]. Testosterone regulates spermatogenesis, maintains the male secondary sexual characteristics, and influences male sexual behavior. It also exerts negative feedback on the hypothalamus and pituitary gland (explained in the forthcoming sections) to regulate the secretion of gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH), thereby maintaining a balanced hormonal environment necessary for reproductive function [10]. Testosterone has several important functions in the male body. It is responsible for the development of male sexual characteristics, such as the growth of facial hair, the deepening of the voice, and the development of the penis and testes during puberty. Testosterone is also involved in the regulation of muscle mass, bone density, and the production of red blood cells [10]. In addition to testosterone, the testes also produce small amounts of other androgens, such as dehydroepiandrosterone (DHEA) and androstenedione. These androgens are converted to testosterone in peripheral tissues, and they also play a role in male sexual development and function [27].
The hypothalamus and pituitary glands are two important components of the endocrine system, which play a critical role in the regulation of the male reproductive system [16]. The hypothalamus secretes GnRH, which stimulates the pituitary gland to secrete follicle-stimulating hormones FSH and LH. These hormones then stimulate the testes to produce testosterone and regulate spermatogenesis [27].
The HPG axis is a complex feedback system, which means that the levels of hormones are constantly monitored and adjusted to maintain homeostasis. When testosterone levels are low, the hypothalamus and pituitary gland increase the production of GnRH, FSH, and LH to stimulate the testes to produce more testosterone. Conversely, when testosterone levels are high, the production of GnRH, FSH, and LH is reduced to prevent overproduction of testosterone [16]. The HPG axis is also responsible for the regulation of the male reproductive system during different stages of life. During puberty, the axis is activated to stimulate the development of male sexual characteristics, including the growth of facial and body hair, the deepening of the voice, and the development of the penis and testes. In adulthood, the HPG axis regulates the production of testosterone and sperm, as well as the maintenance of sexual function [16, 27].
The male reproductive system also includes several accessory glands, which produce secretions that contribute to the seminal fluid. These glands include the seminal vesicles, prostate gland, and bulbourethral glands [9]. The secretions from these glands provide nutrients and lubrication for the sperm, as well as a buffering capacity to protect the sperm from the acidic environment of the female reproductive tract. The secretion of these accessory gland secretions is also regulated by hormones. Testosterone and dihydrotestosterone (DHT) stimulate the secretion of the seminal vesicles and prostate gland, while estrogen stimulates the secretion of the bulbourethral glands [10]. The regulation of these secretions is important for the proper function of the male reproductive system.
Infertility is a condition that affects a considerable number of people worldwide. According to the World Health Organization (WHO), infertility is defined as the inability to conceive after one year of unprotected sexual intercourse [3]. Although infertility is often thought of as a female issue, male infertility is responsible for up to 50% of infertility cases [4]. The causes of male infertility are multifactorial, with a range of genetic, environmental, lifestyle, and medical factors playing a role [6] Fig. (3).
Genetic factors are an important cause of male infertility, with various genetic mutations leading to a range of reproductive abnormalities [28]. The Y chromosome is particularly relevant in male infertility, as it contains many genes involved in male reproductive development [29]. Y chromosome microdeletions, which affect a small portion of the Y chromosome, have been linked to azoospermia (absence of sperm in the ejaculate) and severe oligozoospermia (low sperm count) [30]. In addition, mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which is responsible for regulating ion transport in various tissues, including the male reproductive system, can result in congenital bilateral absence of the vas deferens (CBAVD) [31]. CBAVD is a cause of obstructive azoospermia, where sperm production is normal but cannot be ejaculated due to a blockage in the vas deferens.
Other genetic abnormalities have also been linked to male infertility. For example, mutations in the androgen receptor gene can cause androgen insensitivity syndrome (AIS), where the body is unable to respond to androgen hormones. This can lead to a range of reproductive abnormalities, including hypogonadism, gynecomastia, and azoospermia [32]. Klinefelter syndrome, a condition where males have an extra X chromosome, is also associated with male infertility, with up to 80% of men with Klinefelter syndrome having azoospermia or severe oligozoospermia [33].
Fig. (3)) Causes of male reproductive dysfunctions and infertility.Environmental factors refer to external influences that can contribute to male infertility [34]. These factors may be chemical or physical agents that can have detrimental effects on male reproductive function. Some of the most common environmental factors that have been linked to male infertility include exposure to toxins, radiation, and extreme temperatures [6].
Toxins are chemical substances that can have harmful effects on the male reproductive system. Exposure to environmental toxins has been linked to male infertility by causing damage to the male reproductive organs and reducing sperm count and motility [34]. Chemicals such as pesticides, heavy metals, solvents, and plastics have been implicated in male infertility [35]. For example, exposure to pesticides has been linked to reduced sperm count and motility. Similarly, heavy metals such as lead and mercury can cause DNA damage, which can lead to infertility. Plasticizers such as phthalates and bisphenol A (BPA) have also been linked to male infertility by reducing sperm count and motility [35, 36].
Exposure to radiation can cause damage to the male reproductive organs and reduce sperm count and motility. Radiation therapy used to treat cancer can have a detrimental effect on male fertility by damaging the testes. Exposure to ionizing radiation, such as that from X-rays or nuclear accidents, can also cause DNA damage to sperm and affect male fertility [37].
Exposure to extreme temperatures can also affect male fertility. Prolonged exposure to high temperatures, such as in saunas or hot tubs, can reduce sperm count and motility. Similarly, exposure to low temperatures, such as in cold water or ice, can also have detrimental effects on male fertility [38].
Lifestyle factors refer to behaviors and habits that can contribute to male infertility [39]. These factors can be modified through lifestyle changes and can improve male reproductive function. Some of the most common lifestyle factors that have been linked to male infertility include diet, exercise, smoking, and alcohol consumption.
Diet can play a role in male fertility by providing essential nutrients and antioxidants that support healthy sperm production [39]. A diet that is high in processed foods, trans fats, and sugar has been linked to reduced sperm count and motility. Conversely, a diet that is rich in fruits, vegetables, and whole grains has been associated with improved sperm quality. Antioxidants such as vitamin C, vitamin E, and selenium have also been shown to improve sperm count and motility [40].
Regular exercise can have a positive impact on male fertility by improving blood flow to the reproductive organs and reducing stress levels. However, excessive exercise or training can have the opposite effect and reduce sperm count and motility. Moderate exercise, such as brisk walking or cycling, is recommended to improve male fertility [41].
Smoking is a known risk factor for male infertility. It can reduce sperm count and motility and increase the risk of DNA damage to sperm. Smoking can also affect the quality of semen by decreasing semen volume and altering the pH balance of the reproductive tract [42].
Excessive alcohol consumption can also have a negative impact on male fertility. It can reduce sperm count and motility and increase the risk of DNA damage to sperm. Alcohol can also affect the quality of semen by reducing semen volume and altering the pH balance of the reproductive tract [43].
The causes of male infertility are multifactorial and can be divided into pre-testicular, testicular, and post-testicular factors. Medical conditions and treatments are among the post-testicular factors that can lead to male infertility. This chapter will discuss the medical conditions and treatments that can cause male infertility.
Varicocele: Varicocele is a medical condition characterized by enlarged veins within the scrotum. This condition affects 15% of men and is the most common cause of male infertility [44]. Varicocele can cause a decrease in sperm quality and quantity. The exact mechanism of how varicocele affects sperm production is still unclear. However, studies suggest that varicocele may cause oxidative stress and increase testicular temperature, which can affect sperm production [45].
Infections: Infections of the reproductive tract can lead to male infertility. Sexually transmitted infections such as chlamydia and gonorrhea can cause inflammation and scarring of the reproductive tract, leading to the obstruction of the sperm pathway [46, 47]. Other infections, such as mumps, tuberculosis, and prostatitis, can also affect sperm production and quality [48].
Hormonal Imbalances: Hormonal imbalances can also cause male infertility. The hypothalamic-pituitary-gonadal axis regulates the production of testosterone and sperm [16]. Any disruption in this axis can lead to hormonal imbalances that affect sperm production. Medical conditions such as hypogonadism, hyperprolactinemia, and thyroid disorders can affect the hormonal balance and lead to male infertility [27].
Retrograde Ejaculation: Retrograde ejaculation is a medical condition where semen is ejaculated into the bladder instead of out through the penis. This condition can occur due to nerve damage, medications, or surgery. Retrograde ejaculation can cause male infertility by reducing the number of sperm in the ejaculate [49].
Erectile Dysfunction: Erectile dysfunction is the inability to achieve or maintain an erection during sexual intercourse [50]. This condition can affect fertility by making it difficult for men to have sexual intercourse and ejaculate. Erectile dysfunction can be caused by medical conditions such as diabetes, hypertension, and cardiovascular disease [51].
Chemotherapy: Chemotherapy is a treatment for cancer that uses drugs to kill cancer cells. Chemotherapy can cause male infertility by damaging the testicles and reducing sperm production. The risk of infertility depends on the type and dose of chemotherapy [52].
Radiation Therapy: Radiation therapy is another treatment for cancer that uses high-energy radiation to kill cancer cells. Radiation therapy can also affect sperm production by damaging the testicles. The risk of infertility depends on the dose and location of the radiation [37].
Surgery: Surgery can also cause male infertility. Surgical procedures such as vasectomy and varicocelectomy can lead to obstruction of the sperm pathway and reduce sperm production. In some cases, surgery can also cause nerve damage that leads to retrograde ejaculation [44, 45].
Medications: Some medications can affect sperm production and quality. Medications such as anabolic steroids, antipsychotics, and antidepressants can affect the hormonal balance and reduce sperm production [53]. Chemotherapeutic drugs used to treat autoimmune diseases, such as methotrexate and cyclophosphamide, can also affect sperm production [52].
Immunotherapy: Immunotherapy is a treatment for cancer that uses the immune system of the body to fight cancer cells [53]. Immunotherapy can cause male infertility by damaging the testicles and reducing sperm production. The risk of infertility depends on the type and dose of immunotherapy [54].
The psychological impact of infertility on men is often overlooked, and it can result in emotional distress, anxiety, and depression [55]. This chapter focuses on the psychological impact of male infertility, coping strategies, and the importance of seeking support.
Male infertility is associated with psychological distress that affects the mental health of a man, interpersonal relationships, and overall quality of life [56]. Men with infertility often experience feelings of guilt, shame, and inadequacy, leading to a loss of self-esteem and self-confidence [57]. These feelings can result in depression, anxiety, and stress.
Depression is a common mental health problem among infertile men [55]. In a study conducted by Peterson and colleagues (2003), it was found that men with infertility had higher rates of depression than men without infertility [58]. Depression is a serious mental health condition that can lead to a lack of motivation, loss of interest in activities, and suicidal ideation [55, 59]. Furthermore, anxiety is also a prevalent problem among infertile men. Anxiety is characterized by excessive worry and fear that can interfere with daily activities [60]. Men with infertility often worry about their ability to father a child, the effectiveness of treatments, and the financial cost of fertility treatments [61].
Stress is also a significant problem among men with infertility [62]. Infertility-related stress is caused by various factors such as the time and effort required for fertility treatments, financial burden, and fear of failure [55, 62]. Stress can have a negative impact on the physical health, mental health, and overall well-being of a man [56].
Anger and Frustration: Infertility can also cause men to experience anger and frustration. A study by Peterson and colleagues (2003) found that men with infertility experience more intense anger than their female partners. This anger can be directed toward themselves, their partners, and medical professionals, leading to strained relationships and increased stress [58].
Low Self-Esteem: Male infertility can lead to a decrease in self-esteem and self-worth. Men may feel inadequate, less masculine, or like they are not fulfilling their societal roles. A study by Daniluk and Koert (2008) found that men with infertility report lower self-esteem and feel less in control of their lives.
Coping strategies refer to the psychological mechanisms that individuals use to manage the stress associated with infertility. A study conducted by Peterson et al. (2011) found that coping strategies are important in determining the level of psychological distress experienced by infertile couples [63]. In general, coping strategies can be classified into two types: problem-focused coping and emotion-focused coping. Problem-focused coping strategies refer to efforts to actively address the problem that is causing stress, such as seeking medical treatment for infertility. In the context of male infertility, problem-focused coping strategies might include taking medication to improve sperm quality, undergoing surgery to correct a physical issue, or seeking the advice of a fertility specialist. Emotion-focused coping strategies, on the other hand, involve efforts to manage the emotional distress caused by the problem rather than trying to address the problem itself [64].
There are several emotion-focused coping strategies that can be used to manage the stress associated with male infertility. One such strategy is seeking social support. Research has shown that social support can be an important buffer against the negative psychological consequences of infertility [55]. Social support can come from a variety of sources, including family, friends, and support groups. Support groups can be particularly helpful because they provide a safe and supportive environment where individuals can share their experiences, express their feelings, and receive emotional support from others who are going through the same thing [65]. Another emotion-focused coping strategy is seeking professional help [66]. Infertility can be a very isolating experience, and sometimes, it can be difficult to talk to friends and family about what you are going through. A mental health professional, such as a therapist or counselor, can provide a safe and confidential space to talk about your feelings and work through the emotional challenges of infertility.
Self-care is another important coping strategy [67