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|style="height: 50px; background: #EEEEEE;"| Alcohol abuse in men has been associated with impaired production of testosterone and therefore infertility. <ref name= PMID20090219><pubmed> 20090219</pubmed></ref> One study demonstrated that a typical weekly alcohol consumption of ~40 units resulted in a 33% decrease is spermatazoa concentration. <ref><pubmed>25277121</pubmed></ref> Alcohol abuse adversely affects spermatazoa morphology and production ultimately causing asthenozoospermia and therefore reducing the quality of semen. <ref name= PMID20090219><pubmed>20090219</pubmed></ref>
|style="height: 50px; background: #EEEEEE;"| Alcohol abuse in men has been associated with impaired production of testosterone and therefore infertility. <ref name= PMID20090219><pubmed> 20090219</pubmed></ref> One study demonstrated that a typical weekly alcohol consumption of ~40 units resulted in a 33% decrease is spermatozoa concentration. <ref><pubmed>25277121</pubmed></ref> Alcohol abuse adversely affects spermatozoa morphology and production ultimately causing asthenozoospermia and therefore reducing the quality of semen. <ref name= PMID20090219><pubmed>20090219</pubmed></ref>
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|style="text-align:center; background: #CCEEEE;"| '''Overweight/Obesity'''  
|style="height: 50px; background: #CCEEEE;"| An increase in waist circumference is associated with impaired semen parameters in infertile men. <ref><pubmed>24306102</pubmed></ref> A high body mass index (BMI) is negatively associated with normal spermatazoa morphology, spermatazoa concentration and motility, total spermatazoa count and percentage of vital spermatazoa, therefore negatively affecting male fertility. <ref><pubmed>26067627</pubmed></ref>  
|style="height: 50px; background: #CCEEEE;"| An increase in waist circumference is associated with impaired semen parameters in infertile men. <ref><pubmed>24306102</pubmed></ref> A high body mass index (BMI) is negatively associated with normal spermatozoa morphology, spermatozoa concentration and motility, total spermatozoa count and percentage of vital spermatozoa, therefore negatively affecting male fertility. <ref><pubmed>26067627</pubmed></ref>  
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Revision as of 23:06, 9 October 2015

2015 Student Projects 
2015 Projects: Three Person Embryos | Ovarian Hyper-stimulation Syndrome | Polycystic Ovarian Syndrome | Male Infertility | Oncofertility | Preimplantation Genetic Diagnosis | Students
2015 Group Project Topic - Assisted Reproductive Technology
This page is an undergraduate science embryology student and may contain inaccuracies in either description or acknowledgements.

Male Infertility

Infertility is defined as the inability to achieve a clinical pregnancy after 12 months of unprotected sexual intercourse [1]. Male infertility is the inability for a male to successfully impregnate a fertile female. Infertility is an ever increasing issue that affects one in six Australian couples as reported in the Australian Government Department of Health, National Women's Health Policy. [2] Of these couples who are considered infertile, one in five experience problems that lie solely with the male.

Background Information

Virtual preparation of the spermatozoon showing the acrosome, the nucleus and nuclear envelopes, the mitochondrial sheath of the main piece of the flagellum
Structure of the seminiferous tubule: site of the germination, maturation, and transportation of the sperm cells within the male testes

Structure of spermatozoa

The shape of spermatozoa are suitable for the transport to female gametes via the uterine tube. For this reason the nucleus of the spermatozoa is highly condensed, covered by an acrosome filled with enzymes for establishing contact to the female gamete. The enzyme within the acrosome degrades the zona pellucida of the oocyte (female gamete), allowing membrane fusion. Spermatozoa also consist of a flagellum for progressive motility during the transport throughout the epididymal ducts. The motility is supported by the mitochondrial sheath found in the mid piece of the spermatozoa. [3] [4]

Spermatogenesis

The complete process of male germ cell development is called spermatogenesis, male germ cells develop in the seminiferous tubules of the testes throughout life from puberty to old age. The product of spermatogenesis are mature male gametes called spermatozoa. There are three major stages in spermatogenesis:

1. Spermatogoniogenesis

2. Maturation of spermatocytes

3. Spermiogenesis (which is the cytodifferentiation of spermatids)

Spermatogoniogenesis is the process where spermatogonia multiplicate continuously in successive mitosis. However, the daughter cells will still be interconnected by cytoplasmic bridges and is only dissolved in advanced stages of spermatid development. The stage of meiosis is manifested through changes in the structure of the nucleus after the last spermatogonial division. Cells undergoing meiosis are called spermatocytes. As the process of meiosis comprises two divisions, cells before the first division are called primary spermatocytes and before the second division secondary spermatocytes. During the prophase the duplication of DNA, the condensation of chromosomes, the pairing of homologuous chromosomes and crossing over take place. After division the germ cells become secondary spermatocytes. They do not undergo DNA-replication and divide quickly to the spermatids. This results in four haploid cells, namely the spermatids. These differentiate into mature spermatids, a process called spermiogenesis which ends when the cells are released from the germinal epithelium. At this point, the free cells are called spermatozoa. During spermiogenesis three processes takes place; condensation of the nucleus, formation of acrosome cap filled with enzymes and the development of flagellum structures and their attachment to the head/mid piece of the developing spermatozoa. [5]

Physiology of fertility in Males

Normal reproductive functioning in males is controlled by gonadotropin releasing hormone (GnRH), androgens and gonadatropins. The correct metabolism and functioning of all three types of hormones is essential to the normal and efficient production of spermatazoa, as well as over all reproductive health. GnRH is synthesised and released by the hypothalamus, which stimulates the anterior pituitary to release two gonadatropins: follicle stimulating hormone (FSH) responsible for spermatogenesis in the Sertoli cells and luteinizing hormone (LH) responsible for stimulating the release of androgens by the Leydig cells. Testosterone, the primary androgen, is released into the testes and aids FSH by further promoting spermatogenesis. Furthermore, testosterone is vital to the normal development of many accessory reproductive organs, including the accessory glands. A negative feedback loop of testosterone and inhibin (secreted by Sertoli cells) acts on the anterior pituitary, either decreasing or stimulating the release of FSH and LH. [6]

Male infertility disorders

Types of Male Infertility

Type Description
Oligospermia Low spermatozoon count
Asthenospermia (asthenozoospermia) Reduced motility of spermatozoa within the semen
Teratozoospermia Abnormal spermatozoa morphology within the semen
Oligoasthenozoospermia Combination of reduced motility of spermatozoa (asthenospermia) and low spermatozoa count (oligospermia)
Obstructive Azoospermia Absence of spermatozoa within the semen due to a blockage in the genital tract obstructing the pathway for sperm to enter the penis from the testes
Non-obstructive Azoospermia Absence of spermatozoa within the semen due to sperm producing cells being damaged or destroyed

Causes of Infertility

Due to the increasing rates of male infertility worldwide, researchers have been focusing on aetiological factors for its treatment and prevention. There are numerous causes of male infertility, however, the most common causes are those that relate to the correct development and adequate supply of spermatozoa to result in pregnancy, or inefficient transport of spermatozoa. The three key parameters for assessing male infertility are spermatozoa count, viability and motility[7].

<html5media height="300" width="400">https://www.youtube.com/watch?v=joTrmeDf1dY</html5media> Infertility: Causes Behind Infertility [8]

Major Causes of Male Infertility

Varicocele

Varicocele induced cytoplasmic level apoptosis in animals: inadequate energy supply results in the cells ability to utilise lipids as a secondary energy source to be reduced, therefore reducing normal cellular functioning and division and ultimately leading to cytoplasmic level apoptosis.

Varicocele is one of the leading causes of infertility in males and affects one third of individuals classified as infertile. Varicocele is the abnormal dilation of the internal spermatic veins and creamasteric veins from the panpiniform plexus as a result of back flow of blood. This downward flow of blood into the panpiniform plexus is due to the absence or presence of incomplete valves within the veins. [9] As previously mentioned, the three key markers of spermatozoa quality and of male infertility, spermatozoa viability, count and motility, are also heavily associated with varicocele. [10] Other causes of varicocele include an increase in programmed cell death (apoptosis), increased scrotal temperature of approximately 2.5 degrees Celcius and reduced androgen secretion leading to testosterone deprivation. [11] Testosterone is one of the hormones that play a major role in the correct physiological functioning of the male reproductive system. It is therefore evident that a deprivation of testosterone severely affects the rate of production of spermatozoa, their maturation as well as the male reproductive systems ability to effectively ejaculate semen (related to the development of accessory glands).

Male Reproductive Cancers

Male reproductive cancers, including prostate cancer and testicular cancer, have been shown to dramatically decrease the quality of semen prior to treatment, being comparable with that of infertile and subfertile men. [12] A link between testicular cancer and male infertility has been established by the identification of Testicular Dysgenesis Syndrome (TDS). The improper or abnormal development of the testicles associated with TDS has direct links to Sertoli and Leydig cell disfunction leading to failure of gonocyte maturation and therefore insufficient or low production of mature spermatozoa; one of the key indicators of male infertility. [13]. Furthermore, the presence of tumors in the male reproductive system have systemic effects including immunological and cytotoxic effects on the germinal epithelial leading to reduction in the quality of sperm produced and changes in the processes of spermatogenesis. [14] Finally, it has also been suggested that the fever and malnutrition associated with cancer may lead to alterations in spermatogenesis, a large decrease in spermatozoa concentration and evem azoospermia, the absence of motile spermatozoa. [15]

Chromosomal Abnormalities

Chromosomal Abnormalities are responsible for approximately 5% of all cases of male factor infertility and result in azoospermia (absence of spermatozoa) and oligozoospermia (low spermatozoa concentration). [16] Aneuploidy is the presence of an incorrect number of chromosomes and is the most common error of chromosomal abnormality resulting in infertility. [17] Klinefelter syndrome occurs in approximately 5% of severe oligozoospermic and 10% of azoospermic men and causes the cessation of spermatogenesis at the primary spermatocyte stage. [18] Another aneuploidy associated with male infertility is Y-chromosome microdeletions, present in 10-15% of azoospermic and 5-10% of severe oligozoospermic men, that can result in lack of spermatozoa in ejaculate (AZFa deletion), arrest of spermatogenesis at primary spermatocyte stage (AZFb deletion) and low concentration of spermatozoa (AZFc deletion). [19][20]

Damage to DNA

Factors associated with an increase in the risk of DNA fragmentation resultant in male infertility.

DNA damage in the germ cell population of males has been shown to be a contributing factor to many adverse clinical outcomes including poor semen quality, low fertilisation rates and impaired pre-implantation development; an outcome significant in the use of Assisted Reproductive Technologies when treating infertility. [21] The integrity of spermatzoa can be negatively impacted by deficits in the DNA repair pathways resulting in decrease in germ cell survival and the production of spermatozoa. [22] It has been demonstrated that common inherited variants within genes that encode enzymes utilised in the mismatch repair pathway have a negative relationship with the maintenance of genome integrity, meiotic recombination and even gametogenesis, therefore increasing the risk of DNA damage in spermatozoa and male infertility. [23] Finally, it has been demonstrated that an increase in age is associated with increased spermatozoa DNA damage resulting in a decline in semen volume, spermatozoa motility and morphology and over all semen quality. [24]

Lifestyle Factors

Non-viable spermatozoa: Spermatozoa stained pink by eosin due to a damaged membrane resulting in poor semen quality.

There are numerous lifestyle factors that are associated with a decrease in male fertility that often cause irreversible damage to processes in gametogenesis resulting in poor semen quality. Tobacco smoking has been seen to increase risk of male infertility by up to 30% due to the competitive binding of cadmium to DNA polymerase, replacing zinc and causing damage to the testes. [25] It was also suggested by the same study that excessive alcohol intake has an adverse affect on spermatozoa quality and chromosome number. [25] Another lifestyle factor that produces adverse clinical outcomes to male infertility is obesity and its association with hypogonadatropic hypogonadism; a condition characterised by a decrease in functional activity of the gonads (hormone production and therefore gametogenesis). [26] Studies conducted on animals demonstrates that a sensitivity to leptin in the hypothalamus as a result of obesity, decreases Kiss1 expression, therefore decreasing the release of gonadatropin releasing hormone (GnRH) and ultimately resulting in hypogonadatropic hypogonadism. [26] Studies have demonstrated vigorous physical exercise such as bicycle riding and horse riding, has been associated with urogenital disorders including erectile dysfunction, torsion of the spermatic cord and infertility. [27]

Immunological Infertility

Spermatogenesis commences at puberty after the body has developed a neonatal immune tolerance, therefore, without the necessary and correctly functioning physiological mechanisms such as the blood-testis barrier to separate the spermatozoa from the body's immune response, Sperm-reactive antibodies (SpAb) form and can be found attached to spermatozoa or within the semen. [28] [29] SpAb's have been found present in approximately 5-6% of infertile males.[28] [29] Various microbial pathogens can infect the testes via the circulating blood or the urogenital tract, which can result in orchitis (the inflammation of one or both testicles); characterised by the infiltration of leukocytes into the testes and damage of the seminiferous epithelium, ultimately contributing to male infertility. [30] The disruption of tight junctions within the epididymis, rete testes and even efferent ducts due to inflammation or trauma can result in the exposure of spermatozoa proteins to the immune system and therefore the formation of SpAb's. [28] The presence of SpAb's on the surface of spermatozoa contribute to infertility by causing agglutination in seminal plasma, reduced motility characterised by "shaking" of spermatozoa and even the reduced ability of spermatozoa to penetrate the cervical mucous of the female. [28]

Diagnosis

Male infertility is a widespread condition. There are different diagnostic techniques to detect male infertility, from medical histories, physical examinations to sophisticated tests such as blood tests, ultrasounds and semen analysis. Most cases, there are no obvious signs showing infertility. Sexual intercourse, erections and ejaculations occur usually without any difficulty; the quantity and sperm count of the ejaculated semen are not noticeable with the naked eye.

Infertile patient with arrest of spermatogenesis at the stage of spermatogonia

Physical examination

The physical examination focuses on the size and consistency of the genitals (testicles, epididymus and vas deferens) but also the overall body build. Noting the distribution of body hair and presence or absence of gynecomastia, which is the enlargement of male breasts due to the imbalance of hormones or hormone therapy. In some cases, by examining the size and consistency of the scrotum it is possible to palpate whether or not the epididymis may have hardened from a possible inflammation. Other cases may suggest obstruction within the ducts,this is determined by observing and examining the prostate size and consistency, checking for the presence of cysts or enlarged seminal vesicles.[31] Varicoceles are the most common abnormal finding in infertile men, typically diagnosed by physical examination of Valsalca manoeuvre. It is performed by forceful attempts of exhalation against closed airways by closing one's mouth and pinching their nose while pressing out. This strain increases their intrathoracic pressure and causes the venous return to the heart to decrease and increases the peripheral venous pressure.[32]

Varicoceles can be diagnosed by conducting Valsalva manoeuvre. [33] [10]

Classifications of Valsalva manoeuvre

Grade Description
Grade 1 Varicocele (vein dilatation) only palpable during Valsalva manoeuvre on physical exam
Grade 2 Varicocele palpable on physical exam without Valsalva manoeuvre
Grade 3 Varicocele visible through the scrotal skin without performing Valsalva manoeuvre

Semen Analysis

Although the semen parameters of fertile men can vary, semen analysis is an initial and crucial laboratory test when determining male infertility. [34] Every 2 to 4 weeks, at least two semen samples should be collected. 2 to 4 days prior to the collection is the abstinence period; this is important as it will increase the sperm destiny by 25%. Semen samples are obtained by masturbation or by using a latex free, spermicide free condom during intercourse.

Semen samples are required to liquefy before being studied under the microscope.

Testicular Colour Dopple Ultrasound

High resolution color Doppler ultrasound is a noninvasive means of simultaneously imaging and evaluating the blood flow to the testes in infertile men. It is not generally performed as a routine examination, however physical examination may miss intrascrotal abnormalities readily detected by dopple ultrasound. Non-palpable intrascrotal abnormalities includes testicular and epididymal lesions and tumour. [35]


<pubmed>25038770</pubmed>

<pubmed>21243017</pubmed>

<pubmed>16903932</pubmed>

Risk Factors and Prevention

Risk Factors of Male Infertility

Risk Factors Description
Smoking Semen quality is significantly affected by cigarette smoke. Light smoking has been associated with asthenozoospermia and heavy smoking has been associated with asthenozoospermia, teratozoospermia and oligozoospermia. [36]
Alcohol Consumption Alcohol abuse in men has been associated with impaired production of testosterone and therefore infertility. [37] One study demonstrated that a typical weekly alcohol consumption of ~40 units resulted in a 33% decrease is spermatozoa concentration. [38] Alcohol abuse adversely affects spermatozoa morphology and production ultimately causing asthenozoospermia and therefore reducing the quality of semen. [37]
Overweight/Obesity An increase in waist circumference is associated with impaired semen parameters in infertile men. [39] A high body mass index (BMI) is negatively associated with normal spermatozoa morphology, spermatozoa concentration and motility, total spermatozoa count and percentage of vital spermatozoa, therefore negatively affecting male fertility. [40]
Psychiatric Considerations Stress has been demonstrated to have a negative affect on fertility, reducing testosterone levels and spermatogenesis. [41]
Physical trauma It has been demonstrated that physical traumas and vigorous exercise (often a combination of the two) can result in adverse urogenital disorders such as torsion of the spermatic cord, penile thrombosis, hematuria and infertility. [27]

Treatments

Current treatments for male infertility aim to eliminate the causative factors mentioned above. These may involve improving the male's fertility using drug therapies or surgical procedures, however many assisted reproductive technologies have been introduced and have proven successful. Both methods of treatment have shown evidence of efficacy, thus having great implications on infertile couples worldwide.

Non-surgical Treatments

In order to effectively treat male infertility, it is imperative to correctly identify the specific cause and contributing factors. Currently, the different treatment strategies used or investigated tend to the specific aetiological factors for male infertility. Apart from theoretically allowing natural conception, these treatments also have an implication on the assisted reproductive technologies (ARTs) that are currently available.

Injectable Hormones & Fertility Drugs

Hormonal imbalance is a non-obstructive cause for male infertility. The efficiency of spermatogenesis depends on stimulation and regulation mainly by gonadotropins, GnRH and testosterone, without which may cause infertility. Males that have a deficiency in these hormones are being targeted by research involving injectable hormones such as human chorionic gonadotropin (hCG) and human menopausal gonadotropin (hMG), and Clomiphene citrate, a fertility drug. hCG and hMG are gonadotropins that are used to treat male hypogonadotropic hypogonadism (MHH), a condition associated with infertility causing an underproduction of sperm or testosterone, or both [42]. These gonadotropins have been utilised in infertile males to stimulate the synthesis of testosterone and sperm directly, bypassing the pituitary gland that normally releases gonadoptropins LH and FSH. LH triggers Leydig cells to release testosterone, and FSH plays a vital role in spermatogenesis maintenance as it promotes Sertoli cell maturation [43].

Additionally, clomiphene citrate also increases secretion of GnRH from the hypothalamus, and FSH and LH from the pituitary gland by blocking feedback inhibition of serum estradiol [43]. Normally, males have more testosterone levels than estrogen however those with MHH and consequent infertility, may have the opposite [44]. This was investigated in a study conducted in 2013 by Hussein et al. showing that hCG, hMG and clomiphene citrate are suitable treatments particularly for azoospermia, increasing levels of FSH, LH and total testosterone [43]. Therefore the administration of these substances may correct abnormal hormone levels that contribute to male infertility, thus stimulates spermatogenesis to increase spermatozoa count, motility and viability.

Antioxidants

There has been increasing evidence that infertility may be directly linked to oxidative stress, thus various antioxidants have been experimented with to determine their efficacy as a treatment. Reactive oxygen species (ROS) formed during oxidation plays a vital role in sperm function, particularly in capacitation, acrosome reaction, hyperactivation and sperm-oocyte fusion [45]. In low concentrations, ROS are essential for the synthesis of energy, and contribute to signal transduction pathways within the cell. Usually ROS levels are regulated by natural antioxidants within the seminal plasma [45]. However an influx of ROS and/or a deficiency in antioxidants due to abnormal sperm or environmental stress, can lead to oxidative stress. Spermatozoal cell membranes contain high amounts of polyunsaturated fatty acids that consist of several electron-containing double bonds. The electrons of these fatty acids contribute to the formation of ROS and oxidative stress, thus causing a disruption in the flexibility of the spermatozoal membrane and diminishing the motility and sustainability of sperm [46]. This may result in sperm membrane lipid peroxidation, DNA fragmentation, and apoptosis [45]. The following are a few antioxidants that have been proven to treat oxidative stress, hence improves male fertility.

1. Carotenoids

Carotenoids are naturally occurring pigments produced by plants, algae, and photosynthetic bacteria [47]. They can be divided into 2 different categories based on their chemical composition including carotenes that contain oxygen, and xanthophylls that only contain hydrocarbons [47]. The main source of these chemical compounds in the human diet are from fruits and vegetables as they give them their yellow, red and orange pigments. The role of carotenoids within the healthcare industry are forever growing as they have been suggested supplements for the human body, and as treatments for various cancers and possibly infertility disorders [48]. The antioxidant activity of carotenoids is performed by quenching (deactivating) singlet oxygen that is formed during photosnythesis by plants.
Proposed Mechanisms of Lycopene Treatment for Idiopathic Male Infertility
Lycopenes are a type of carotene carotenoid that is found in various fruits and vegetables such as tomatoes and watermelon. Despite it being a source of vitamin A, it also possesses strong antioxidant properties as it is one of the most effective quenchers of singlet oxygen [49]. Although the exact mechanism of lycopenes is yet to be known, they have a role inneutralizing ROS and hindering their activity, achieved by their ability to donate an electron to free radicals [46]. As a result of this antioxidation pathway, lipid peroxidation is inhibited allowing for spermatozoal membranes to be retained and protected from further damage. Lycopenes have also been suggested to increase natural antioxidant enzymes indirectly, and also decrease the production of pro-inflammatory agents.
Astaxanthin is a keto-carotenoid produced naturally from the microalgae Hematococcus pluvialis [50]. Due to its higher antioxidant activity in comparison to vitamin E, a fat solube antioxidant found in soybean and margarine, it has been suggested as an effective treatment and supplement for male factor infertility. An experimental trial to test Astaxanthin’s influence on sperm function was carried out in 2005 in 27 infertile men [51]. It was found that Astaxanthin allowed for the following:
  • Increased motility concentration
  • Improved sperm morphology and motility
  • Decrease in ROS and Inhibin B (a regulator of spermatogenesis) levels
Model of the Activities of Cerium Dioxide Nanoparticles

2. Cerium dioxide nanoparticles (CNPs)

Cerium dioxide nanoparticles have been used extensively in the health care industry as potential pharmacological agents to treat various conditions from cancer to male infertility. These products are formed by cerium combining to oxygen obtaining a strong crystalline structure [52]. CNPs have the ability to interchange Ce 3+ and Ce 4+ ions that are present on its surface, leading to defects in oxygen within its crystal lattice structure. These regions on the surface of CNPs are ‘reactive sites’ to attract free radicals [53]. A research team experimented on male rats to observe CNP effects on male health and infertility, providing further evidence that oxidative stress plays a key role in preventing proper spermatogenesis [53]. Therefore, the electronic structure of CNPs, and thus its antioxidant properties make this material a promising therapeutic for male infertility caused or affected by oxidative stress.

3. Vitamin E and C

Vitamin E is a fat – soluble antioxidant that exists in 8 chemical forms of different biological activity. The only form of vitamin E required by the human body is alpha-tocopherol [54]. This chemical compound is found in various foods such as wheat germ oil, sunflower seeds and oil, and almonds [55]. Currently, the recommended dietary allowance (RDA) of vitamin E is 15 mg with an adult maximum of 1000 mg [55]. Due to the ability for vitamin E to prevent the peroxidation of PUFA, it has extremely positive implications on infertile men as spermatozoa have high levels of these compounds. From previous studies, vitamin E (alpha – tocopherol) levels decreased to 66.54% and 66.04% in oligospermic and azoospermic males respectively compared to fertile men [56]. Therefore there is a positive association between alpha – tocopherol levels and sperm count and motility .
On the other hand, vitamin C is a water-soluble antioxidant [57]. As an electron donor it neutralizes free radicals and also prevents ROS synthesis. As the human body does not produce or store vitamin C, daily intakes of vitamin C – containing foods are required to maintain its levels internally. Such foods with the highest vitamin C content include citrus fruits (oranges), kiwi fruit, broccoli and cauliflower. The RDA for vitamin C in male adults is 90mg/day [57]. A study published in March 2015 demonstrated that infertile men administered with vitamin C had a significantly better sperm motility rate and morphology. Although it had little/no effect on sperm count, it is still a well recognizable and effective treatment for male infertility [58].

Traditional Chinese Medicine

More recently discovered treatments for male infertility involve the hollistic principles of traditional Chinese medicine (TCM). Disregarding the conventional medicines more commonly prescribed in today’s society, the effects of Chinese herbal therapy, massage and acupuncture, have been suggested to improve sperm motility and viability of infertile males [59]. Acupuncture and massage has been proven to alleviate stress, increase blood flow to reproductive organs, regulate the immune system, and improve dysfunctions in male infertility [59].

Additionally, Chinese herbal medicines have been widely used in experiments to prove their beneficial effects on treating infertility. The following are examples of a few herbal therapies that have been investigated.

Examples of Chinese Herbal Therapies

Herb Evidence
Yi Kang Decoction 100 immune infertile males treated with this herb had greater sperm motility, agglutination, and overall increased pregnancy rates in comparison to prednisone, a steroid that reduces sperm antibody levels [60]
Hu Zhang Dan Shen Yin 60 treated infertile men showed a higher antisperm antibody reversing ratio than prednisone, thus allows for greater sperm production [61]
Zhibai Dihuang This herb was used to treat 80 cases of male immune infertility in the form of a pill, resulting in increased sperm motility and viability [62]

Surgical Treatments

Varicocele Surgery

Varicocele repair can be performed by either percutaneous radiographic embolization or surgery to correct male infertility [10]. The desired outcome of these procedures is to lower the temperature of the scrotum for normal spermatogenesis to occur.

Percutaneous radiographic embolization involves the catheterization of the internal spermatic vein and its occlusion using a sclerosant (injectable irritant) or solid embolic devices such as stainless steel coils [63]. The administration of the sclerosant and solid embolic devices are given at the level of the inguinal crease and ligament respectively to prevent the backflow of blood into the pampiniform plexus. This method is much less invasive than surgical procedures and has very high success rates, and low recurrence rates [63].

As for the surgical approach, these methods are far more invasive but variable in terms of success rates and recurrence. It is important to note that all of these varicocele repair methods, surgery and embolisation, aim to impede increasing temperature of the scrotum caused by the pampiniform plexus.

Surgical Approach to Varicocele Repair

Surgical Method of Varicocele Repair Description
Inguinal Surgery
  • Involves opening the inguinal canal and the incision of the varicocele vein [10]
  • Allows preservation of lymphatic vessels
  • Takes longer to heal
Subinguinal Surgery
  • Incision below external inguinal ring
  • Less pain due to the area of incision as it avoids the aponeurosis (flat tendon) of the abdominal external oblique muscle [10]
Retroperitoneal Surgery
  • Ligation of the internal spermatic vein
  • Can be performed as a mass ligation involving the artery, vein and lymphatic vessels, or artery sparing ligation preserving lymphatic vessels [10]
Laparoscopic Varicocelectomy
  • At the level of the internal inguinal ring, the internal spermatic vein is ligated while sparing the corresponding artery [64]
  • Allows for a more accurate identification of vessels within the area

Ejaculatory Duct Resection

Vasectomy Reversal

Male Infertility Treatments with Assisted Reproductive Technologies (ARTs)

It is known that males with fertility problems have little/no chance of conceiving a child with a woman. To address this issue many ARTs have been developed to allow for a successful pregnancy, which all involve the process of sperm retrieval.


Intrauterine Insemination (IUI)

In Vitro Fertilisation (IVF)

Intracytoplasmic Sperm Injection (ICSI)

Some ARTs allow for the male's genetic material to be passed onto the offspring, contingent upon a successful sperm extraction/retrieval such as intracytoplasmic sperm injection (ICSI). Although only a spermatozoon (single sperm) is required for this particular procedure, these treatment methods ultimately aim to "maximize the sperm retrieval yield" [43].

References

  1. The World Health Organisation,. (2015). Human Reproductive Programme | Sexual and Reproductive Health. Retrieved 4 September 2015, from http://www.who.int/reproductivehealth/topics/infertility/definitions/en/
  2. The Department of Health,. (2011). Department of Health | Fertility and infertility. Health.gov.au. Retrieved 2 September 2015, from http://www.health.gov.au/internet/publications/publishing.nsf/Content/womens-health-policy-toc~womens-health-policy-experiences~womens-health-policy-experiences-reproductive~womens-health-policy-experiences-reproductive-maternal~womens-health-policy-experiences-reproductive-maternal-fert
  3. <pubmed>14617369</pubmed>
  4. Holstein AF, Roosen-Runge EC. Atlas of Human Spermatogenesis. Berlin: Grosse; 1981
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  6. Stanfield, L. C. Pearson New International Edition Principles of Human Physiology Fifth Edition
  7. <pubmed>21243017</pubmed>
  8. St Pete Urology. (2011, September 14) Infertility: Causes Behind Infertility. Retrieved from https://www.youtube.com/watch?v=joTrmeDf1dY
  9. Marmar, L.J. (2001) Varicocele and Male Infertility Part II: The pathophysiology of varicoceles in the light of current molecular and genetic information. Human Reproduction Update, Vol. 7, No. 5 pp. 461-472 retrieved 2nd September 2015, from http://humupd.oxfordjournals.org/content/7/5/461.long
  10. 10.0 10.1 10.2 10.3 10.4 10.5 Cocuzzo, M. Cocuzzo, M. A. Bragais, F. M/ P. Agarwal, A. (2008) The role of varicocele repair in the new era of assisted reproductive technologies. Clinics Vol. 63, No. 6 retrieved 2nd September 2015, from http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1807-59322008000300018&lng=en&nrm=iso&tlng=en
  11. Marmar, L.J. (2001) Varicocele and Male Infertility Part II: The pathophysiology of varicoceles in the light of current molecular and genetic information. Human Reproduction Update, Vol. 7, No. 5 pp. 461-472 retrieved 2nd September 2015, from http://humupd.oxfordjournals.org/content/7/5/461.long
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