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Medical condition
Male infertility
Male infertility refers to a male's inability to cause pregnancy in a fertile female. In humans it accounts for 40–50% of infertility.[1][2][3] It affects approximately 7% of all men.[4] Male infertility is commonly due to deficiencies in the semen, and semen quality is used as a surrogate measure of male fecundity.[5]
Antisperm antibodies (ASA) have been considered as infertility cause in around 10–30% of infertile couples.[7] ASA production are directed against surface antigens on sperm, which can interfere with sperm motility and transport through the female reproductive tract, inhibiting capacitation and acrosome reaction, impaired fertilization, influence on the implantation process, and impaired growth and development of the embryo. Risk factors for the formation of antisperm antibodies in men include the breakdown of the blood‑testis barrier, trauma and surgery, orchitis, varicocele, infections, prostatitis, testicular cancer, failure of immunosuppression and unprotected receptive anal or oral sex with men.[7][8]
Testicular factors refer to conditions where the testes produce sperm of low quantity and/or poor quality despite adequate hormonal support and include:
Varicocele, is a condition of swollen testicle veins. It is present in 15% of normal men and in about 40% of infertile men. It is present in up to 35% of cases of primary infertility and 69-81% of secondary infertility.[9]
Pre-testicular factors refer to conditions that impede adequate support of the testes and include situations of poor hormonal support and poor general health including:
Obesity increases the risk of hypogonadotropic hypogonadism.[14] Animal models indicate that obesity causes leptin insensitivity in the hypothalamus, leading to decreased Kiss1 expression, which, in turn, alters the release of gonadotropin-releasing hormone (GnRH).[14]
Undiagnosed and untreated coeliac disease (CD). Coeliac men may have reversible infertility. Nevertheless, CD can present with several non-gastrointestinal symptoms that can involve nearly any organ system, even in the absence of gastrointestinal symptoms. Thus, the diagnosis may be missed, leading to a risk of long-term complications.[15] In men, CD can reduce semen quality and cause immature secondary sex characteristics, hypogonadism and hyperprolactinaemia, which causes impotence and loss of libido.[16] The giving of gluten free diet and correction of deficient dietary elements can lead to a return of fertility.[15][16] It is likely that an effective evaluation for infertility would best include assessment for underlying celiac disease, both in men and women.[17]
There is increasing evidence that the harmful products of tobacco smoking may damage the testicles[19] and kill sperm,[20][21] but their effect on male fertility is not clear.[22] Some governments require manufacturers to put warnings on packets. Smoking tobacco increases intake of cadmium, because the tobacco plant absorbs the metal. Cadmium, being chemically similar to zinc, may replace zinc in the DNA polymerase, which plays a critical role in sperm production. Zinc replaced by cadmium in DNA polymerase can be particularly damaging to the testes.[23]
Common inherited variants in genes that encode enzymes employed in DNA mismatch repair are associated with increased risk of sperm DNA damage and male infertility.[24] As men age there is a consistent decline in semen quality, and this decline appears to be due to DNA damage.[25] The damage manifests by DNA fragmentation and by the increased susceptibility to denaturation upon exposure to heat or acid, the features characteristic of apoptosis of somatic cells.[26] These findings suggest that DNA damage is an important factor in male infertility.
An increasing amount of recent evidence has been recorded documenting abnormal sperm DNA methylation in association with abnormal semen parameters and male infertility.[27][28]
Post-testicular factors decrease male fertility due to conditions that affect the male genital system after testicular sperm production and include defects of the genital tract as well as problems in ejaculation:
The diagnosis of infertility begins with a medical history and physical exam by a physician, physician assistant, or nurse practitioner. Typically two separate semen analyses will be required. The provider may order blood tests to look for hormone imbalances, medical conditions, or genetic issues.
The past medical or surgical history may reveal thyroid or liver disease (abnormalities of spermatogenesis), diabetic neuropathy (retrograde ejaculation), radical pelvic or retroperitoneal surgery (absent seminal emission secondary to sympathetic nerve injury), or hernia repair (damage to the vas deferens or testicular blood supply).
Usually, the patient disrobes completely and puts on a gown. The physician, physician assistant, or nurse practitioner will perform a thorough examination of the penis, scrotum, testicles, I vas deferens, spermatic cords, ejaculatory ducts, urethra, urinary bladder, anus and rectum. An orchidometer can measure testicular volume, which in turn is tightly associated with both sperm and hormonal parameters.[4] A physical exam of the scrotum can reveal a varicocele, but the impact of detecting and surgically correct a varicocele on sperm parameters or overall male fertility is debated.[4]
The volume of the semen sample, approximate number of total sperm cells, sperm motility/forward progression, and % of sperm with normal morphology are measured. This is the most common type of fertility testing.[29][30] Semen deficiencies are often labeled as follows:
Leucospermia - a high level of white blood cells in semen
Normozoospermia or Normospermia - It is a result of semen analysis that shows normal values of all ejaculate parameters by WHO but still there are chances of being infertile. This is also called as Unexplained Infertility [31]
There are various combinations of these as well, e.g. Teratoasthenozoospermia, which is reduced sperm morphology and motility. Low sperm counts are often associated with decreased sperm motility and increased abnormal morphology, thus the terms "oligoasthenoteratozoospermia" or "oligospermia" can be used as a catch-all.
Scrotal ultrasonography is useful when there is a suspicion of some particular diseases. It may detect signs of testicular dysgenesis, which is often related to an impaired spermatogenesis and to a higher risk of testicular cancer.[4] Scrotum ultrasonography may also detect testicular lesions suggestive of malignancy. A decreased testicular vascularization is characteristic of testicular torsion, whereas hyperemia is often observed in epididymo-orchitis or in some malignant conditions such as lymphoma and leukemia.[4]Doppler ultrasonography useful in assessing venous reflux in case of a varicocele, when palpation is unreliable or in detecting recurrence or persistence after surgery, although the impact of its detection and surgical correction on sperm parameters and overall fertility is debated.[4]
Dilation of the head or tail of the epididymis is suggestive of obstruction or inflammation of the male reproductive tract.[4] Such abnormalities are associated with abnormalities in sperm parameters, as are abnormalities in the texture of the epididymis.[4] Scrotal and transrectal ultrasonography (TRUS) are useful in detecting uni- or bilateral congenital absence of the vas deferens (CBAVD), which may be associated with abnormalities or agenesis of the epididymis, seminal vesicles or kidneys, and indicate the need for testicular sperm extraction.[4] TRUS plays a key role in assessing azoospermia caused by obstruction, and detecting distal CBAVD or anomalies related to obstruction of the ejaculatory duct, such as abnormalities within the duct itself, a median cyst of the prostate (indicating a need for cyst aspiration), or an impairment of the seminal vesicles to become enlarged or emptied.[4]
Maintaining optimal frequency of coital activity: sperm counts can be depressed by daily coital activity[33] and sperm motility may be depressed by coital activity that takes place too infrequently (abstinence 10–14 days or more).[33]
Diet: Healthy diets (i.e. the Mediterranean diet) rich in such nutrients as omega-3 fatty acids, some antioxidants and vitamins, and low in saturated fatty acids (SFAs) and trans-fatty acids (TFAs) are inversely associated with low semen quality parameters. In terms of food groups, fish, shellfish and seafood, poultry, cereals, vegetables and fruits, and low-fat dairy products have been positively related to sperm quality. However, diets rich in processed meat, soy foods, potatoes, full-fat dairy products, coffee, alcohol and sugar-sweetened beverages and sweets have been inversely associated with the quality of semen in some studies. The few studies relating male nutrient or food intake and fecundability also suggest that diets rich in red meat, processed meat, tea and caffeine are associated with a lower rate of fecundability. This association is only controversial in the case of alcohol. The potential biological mechanisms linking diet with sperm function and fertility are largely unknown and require further study.[34]
Treatments vary according to the underlying disease and the degree of the impairment of the male fertility. Further, in an infertility situation, the fertility of the female needs to be considered.
Pre-testicular conditions can often be addressed by medical means or interventions.
Obstructive causes of post-testicular infertility can be overcome with either surgery or IVF-ICSI. Ejaculatory factors may be treatable by medication, or by IUI therapy or IVF.
Vitamin E helps counter oxidative stress,[35] which is associated with sperm DNA damage and reduced sperm motility.[36] A hormone-antioxidant combination may improve sperm count and motility.[37] However, there is only some low quality evidence from few small studies that oral antioxidants given to males in couples undergoing in vitro fertilisation for male factor or unexplained subfertility result in higher live birth rate.[38] It is unclear if there are any adverse effects.[38]
Though androgens are absolutely essential for spermatogenesis and therefore male fertility, exogenous testosterone therapy has been found to be ineffective in benefiting men with low sperm count.[41] This is thought to be because very high local levels of testosterone in the testes (concentrations in the seminiferous tubules are 20- to 100-fold greater than circulating levels)[42] are required to mediate spermatogenesis, and exogenous testosterone therapy (which is administered systemically) cannot achieve these required high local concentrations (at least not without extremely supraphysiological dosages).[41] Moreover, exogenous androgen therapy can actually impair or abolish male fertility by suppressing gonadotropin secretion from the pituitary gland, as seen in users of androgens/anabolic steroids (who often have partially or completely suppressed sperm production).[39][41] This is because suppression of gonadotropin levels results in decreased testicular androgen production (causing diminished local concentrations in the testes)[39][41] and because FSH is independently critical for spermatogenesis.[43][44] In contrast to FSH, LH has little role in male fertility outside of inducing gonadal testosterone production.[45]
Estrogen, at some concentration, has been found to be essential for male fertility/spermatogenesis.[46][47] However, estrogen levels that are too high can impair male fertility by suppressing gonadotropin secretion and thereby diminishing intratesticular androgen levels.[41] As such, clomiphene citrate (anantiestrogen) and aromatase inhibitors such as testolactoneoranastrozole have shown effectiveness in benefiting spermatogenesis.[41]
Low-dose estrogen and testosterone combination therapy may improve sperm count and motility in some men,[48] including in men with severe oligospermia.[49]
Researchers at Münster University developed in vitro culture conditions using a three-dimensional agar culture system which induces mouse testicular germ cells to reach the final stages of spermatogenesis, including spermatozoa generation.[50] If reproduced in humans, this could potentially enable infertile men to father children with their own sperm.[51][52]
Researchers from Montana State University developed precursors of sperm from skin cells of infertile men.[53][54][55]
Sharpe et al. comment on the success of intracytoplasmic sperm injection (ICSI) in women saying, "[t]hus, the woman carries the treatment burden for male infertility, a fairly unique scenario in medical practice. Ironically, ICSI's success has effectively diverted attention from identifying what causes male infertility and focused research onto the female, to optimize the provision of eggs and a receptive endometrium, on which ICSI's success depends."[56][57]
There are a variety of social stigmas that surround male infertility throughout the world. A lot of research has pointed to the relationship between infertility and emasculation. [58][59][60] In places like Egypt[59], Zimbabwe[58], and Mexico[61], erectile dysfunction also known as impotence, is considered a determinant of infertility. When stereotypical ideals of manhood are virility and strength, men who face problems of fertility tend to feel inadequate and sometimes even suicidal [62]. In many cases, a variety of socio-economic interventions come in play to determine penile activity. While doing so, it publicizes a private matter and reinforce an emasculating condition. For the Shona people, since impotence is linked to infertility, an examination to check on the penile function spans from infancy to post marriage [58]. At infancy, there are daily check-ups by the mothers on the son's erection and urine quality. When the son reaches puberty, they are asked to ejaculate in river banks and for their male elders to examine sperm quality. The traditions last until post-marriage, when the family of the bride take part to check on consummation and the groom's sperm quality.
^Cooper TG, Noonan E, Von Eckardstein S, Auger J, Baker HW, Behre HM, Haugen TB, Kruger T, Wang C (2009). "World Health Organization reference values for human semen characteristics". Human Reproduction Update. 16 (3): 231–45. doi:10.1093/humupd/dmp048. PMID19934213.
^Rowe PJ, Comhaire FH, Hargreave TB, Mahmoud AM (2000). "Chapter 2: History taking". WHO manual for the standardized investigation, diagnosis and management of the infertile male. Cambridge [England]: Published on behalf of the World Health Organization by Cambridge University Press. pp. 5–16. ISBN0-521-77474-8.
^Zhang J, Qiu SD, Li SB, Zhou DX, Tian H, Huo YW, Ge L, Zhang QY (2007). "Novel mutations in ubiquitin-specific protease 26 gene might cause spermatogenesis impairment and male infertility". Asian Journal of Andrology. 9 (6): 809–14. doi:10.1111/j.1745-7262.2007.00305.x. PMID17968467.
^ abTeerds KJ, de Rooij DG, Keijer J (2011). "Functional relationship between obesity and male reproduction: from humans to animal models". Hum. Reprod. Update. 17 (5): 667–83. doi:10.1093/humupd/dmr017. PMID21546379.
^ abHozyasz, K (Mar 2001). "Coeliac disease and problems associated with reproduction". Ginekol Pol. 72 (3): 173–9. PMID11398587.
^Leibovitch I, Mor Y (2005). "The Vicious Cycling: Bicycling Related Urogenital Disorders". European Urology. 47 (3): 277–86, discussion 286–7. doi:10.1016/j.eururo.2004.10.024. PMID15716187.
^Thompson J, Bannigan J (Apr 2008). "Cadmium: toxic effects on the reproductive system and the embryo". Reprod Toxicol (Review). 25 (3): 304–15. doi:10.1016/j.reprotox.2008.02.001. PMID18367374.
^Agarwal A, Prabakaran SA, Said TM (2005). "Prevention of Oxidative Stress Injury to Sperm". Journal of Andrology. 26 (6): 654–60. doi:10.2164/jandrol.05016. PMID16291955.
^Robbins WA, Elashoff DA, Xun L, Jia J, Li N, Wu G, Wei F (2005). "Effect of lifestyle exposures on sperm aneuploidy". Cytogenetic and Genome Research. 111 (3–4): 371–7. doi:10.1159/000086914. PMID16192719.
^Gorczyca W, Traganos F, Jesionowska H, Darzynkiewicz Z (July 1993). "Presence of DNA strand breaks and increased sensitivity of DNA in situ to denaturation in abnormal human sperm cells: analogy to apoptosis of somatic cells". Experimental Cell Research. 207 (1): 202–5. doi:10.1006/excr.1993.1182. PMID8391465.
^Kenneth I. Aston; Philip J. Uren; Timothy G. Jenkins; Alan Horsager; Bradley R. Cairns; Andrew D. Smith; Douglas T. Carrell (December 2015). "Aberrant sperm DNA methylation predicts male fertility status and embryo quality". Fertility and Sterility. 104 (6): 1388–1397. doi:10.1016/j.fertnstert.2015.08.019. PMID26361204.
^Hargreave TB, McGowan B, Harvey J, McParland M, Elton RA (April 1986). "Is a male infertility clinic of any use?". Br. J. Urol. 58 (2): 188–93. doi:10.1111/j.1464-410x.1986.tb09024.x. PMID3697634.
^ abcdSperoff L, Glass RH, Kase NG (1999). Clinical Endocrinology and Infertility (6th ed.). Lippincott Williams and Wilkins. p. 1085. ISBN0-683-30379-1.
^Salas-Huetos A, Bulló M, Salas-Salvadó J (July 2017). "Dietary patterns, foods and nutrients in male fertility parameters and fecundability: a systematic review of observational studies". Human Reproduction Update. 23 (4): 371–389. doi:10.1093/humupd/dmx006. PMID28333357.
^Ghanem H, Shaeer O, El-Segini A (2010). "Combination clomiphene citrate and antioxidant therapy for idiopathic male infertility: A randomized controlled trial". Fertility and Sterility. 93 (7): 2232–5. doi:10.1016/j.fertnstert.2009.01.117. PMID19268928.
^Pasqualotto FF, Fonseca GP, Pasqualotto EB (2008). "Azoospermia after treatment with clomiphene citrate in patients with oligospermia". Fertility and Sterility. 90 (5): 2014.e11–2. doi:10.1016/j.fertnstert.2008.03.036. PMID18555230.
^Liu YX (2005). "Control of spermatogenesis in primate and prospect of male contraception". Arch. Androl. 51 (2): 77–92. doi:10.1080/01485010490485768. PMID15804862.
^Fody EP, Walker EM (1985). "Effects of drugs on the male and female reproductive systems". Ann. Clin. Lab. Sci. 15 (6): 451–8. PMID4062226.
^O'Donnell L, Robertson KM, Jones ME, Simpson ER (2001). "Estrogen and spermatogenesis". Endocr. Rev. 22 (3): 289–318. doi:10.1210/edrv.22.3.0431. PMID11399746.
^Carreau S, Bouraima-Lelong H, Delalande C (2012). "Role of estrogens in spermatogenesis". Front Biosci. 4: 1–11. doi:10.2741/356. PMID22201851.
^Sah P (1998). "Role of low-dose estrogen–testosterone combination therapy in men with oligospermia". Fertility and Sterility. 70 (4): 780–1. doi:10.1016/S0015-0282(98)00273-8. PMID9797116.
^ abInhorn, Marcia (2004). "Middle Eastern Masculinities in the Age of New Reproductive Technologies: Male Infertility and Stigma in Egypt and Lebanon". Medical Anthropology Quarterly. 18 (2): 162–182. doi:10.1525/maq.2004.18.2.162. PMID15272802 – via JSTOR.
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