Factors relating to<unk>  include: Immune<unk>  Antisperm antibodies (ASA) have been considered as<unk>  cause in around 10–30% of infertile couples. 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. Genetics Chromosomal anomalies and genetic mutations account for nearly 10–15% of all<unk>  cases. Klinefelter syndrome One of the most commonly known causes of<unk>  is Klinefelter syndrome, affecting 1 out of 500–1000 newborn males Klinefelter syndrome is a chromosomal defect that occurs during gamete formation due to a non-disjunction error during cell division. Resulting in males having smaller testes, reducing the amount of testosterone and sperm production. Males with this syndrome carry an extra X chromosome (XXY), meaning they have 47 chromosomes compared to the normal 46 in each cell. This extra chromosome directly affects sexual development before birth and during puberty (links to learning disabilities and speech development have also been shown to be affected). There are varieties in Klinefelter syndrome, where some cases may have the extra X chromosome in some cells but not others, referred to as mosaic Klinefelter syndrome, or where individuals have the extra X chromosome in all cells. The reduction of testosterone in the male body normally results in an overall decrease in the production of viable sperm for these individuals thereby forcing them to turn to fertility treatments to father children. Y chromosome deletions Y chromosomal<unk>  is a direct cause of<unk>  due to its effects on sperm production, occurring in 1 out of every 2000 males. Usually affected men show no sign of symptoms other than at times can exhibit smaller teste size. Men with this condition can exhibit azoospermia (no sperm production), oligozoospermia (small number of sperm production), or they will produce abnormally shaped sperm (teratozoospermia). This case of<unk>  occurs during the development of gametes in the male, where a normal healthy male will produce both X and a Y chromosome, affected males have genetic deletions in the Y chromosome. These deletions affect protein production that is vital for spermatogenesis. Studies have shown that this is an inherited trait; if a male is fathered by a man who also exhibited y chromosome deletions then this trait will be passed down. These individuals are thereby “Y-linked”, although daughters are not affected due to the lack of the Y chromosome. Other * Age group 12-49 (see also: Paternal age effect) * Abnormal set of chromosomes * Centriole * Neoplasm, e.g. seminoma * Idiopathic failure * Cryptorchidism * Trauma * Hydrocele * Hypopituitarism in adults, and hypopituitarism untreated in children (resulting in growth hormone deficiency and proportionate dwarfism.) * Mumps * Malaria * Testicular cancer * Defects in USP26 in some cases * Acrosomal defects affecting egg penetration * Idiopathic oligospermia - unexplained sperm deficiencies account for 30% of<unk> . Pre-testicular causes 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: Varicocele 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<unk>  and 69–81% of secondary<unk> . * Hypogonadotropic hypogonadism due to various causes * Obesity increases the risk of hypogonadotropic hypogonadism. 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). * Undiagnosed and untreated coeliac disease (CD). Coeliac men may have reversible<unk> . 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. In men, CD can reduce semen quality and cause immature secondary sex characteristics, hypogonadism and hyperprolactinaemia, which causes impotence and loss of libido. The giving of gluten free diet and correction of deficient dietary elements can lead to a return of fertility. It is likely that an effective evaluation for<unk>  would best include assessment for underlying celiac disease, both in men and women. * Drugs, alcohol * Strenuous riding (bicycle riding, horseback riding) * Medications, including those that affect spermatogenesis such as chemotherapy, anabolic steroids, cimetidine, spironolactone; those that decrease FSH levels such as phenytoin; those that decrease sperm motility such as sulfasalazine and nitrofurantoin * Genetic abnormalities such as a Robertsonian translocation Tobacco smoking There is increasing evidence that the harmful products of tobacco smoking may damage the testicles and kill sperm, but their effect on male fertility is not clear. 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. DNA damage Common inherited variants in genes that encode enzymes employed in DNA mismatch repair are associated with increased risk of sperm DNA damage and<unk> . As men age there is a consistent decline in semen quality, and this decline appears to be due to DNA damage. 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. These findings suggest that DNA damage is an important factor in<unk> . Epigenetic An increasing amount of recent evidence has been recorded documenting abnormal sperm DNA methylation in association with abnormal semen parameters and<unk> . Until recently, scientists have thought that epigenetic markers only affect the individual and are not passed down due to not changing the DNA. New studies suggest that environmental factors that changed an individual's epigenetic markers can be seen in their grandchildren, one such study demonstrating this through rats and fertility disruptors. Another study bred rats exposed to an endocrine disruptor, observing effects up to generation F5 including decreased sperm motility and decreased sperm count. These studies suggest that environmental factors that influence fertility can be felt for generations even without changing the DNA. Post-testicular causes 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: * Vas deferens obstruction * Lack of Vas deferens, often related to genetic markers for cystic fibrosis * Infection, e.g. prostatitis, male accessory gland infection * Retrograde ejaculation * Ejaculatory duct obstruction * Hypospadias * Impotence
Male infertility
Oncofertility
Female infertility
Infertility
Ejaculation disorders
Chronic testicular pain
Delayed puberty
Late-onset hypogonadism