Medical research continues to try to understand the causes of male fertility problems and about forty percent of men are responsible for infertility in their marriage. it has been discovered that constant use of laptop decreases the infertility rate in both male and female. Male infertility is usually caused by problems that affect either sperm production or sperm transport. Through medical testing, the doctor may be able to find the cause of the problem.
1. INFECTIONS.
Poorly treated sexually transmitted disease can become resistant to drugs. syphilis, chlamydia, gonorrhea, staphylococcus, etc. are some of the infections that can destroy male sperm if they are poorly treated. All male sexually transmitted infections should be treated by qualified doctors. The role of infection in idiopathic male infertility has been underestimated, in particular chronic asymptomatic chlamydial infections. Chlamydia can reside in the epididymis and vas deferens, affecting oligozoospermia development and fertility. One study suggests that approximately 28-71 percent of infertile men have evidence of a chlamydial infection. The presence of anti-sperm antibodies may indicate an undiagnosed infection, and is estimated to be a relative cause of infertility in 3-7 percent of cases. In a study designed to examine the effects of antioxidants on anti-sperm antibodies, there was a significant correlation between beta carotene levels and antibody titers, suggesting dietary antioxidants are involved in mediating immune function in the male reproductive system.
2. DIETARY AND LIFESTYLE FACTORS.
In addition to avoiding exogenous estrogens and pesticides, there are other dietary factors to consider. Adequate intake of essential fatty acids is important to ensure proper membrane fluidity and energy production in sperm cells. High dietary intake of hydrogenated oils, particularly cottonseed oil, has been shown to have a negative impact on sperm cell function. Not only does cottonseed oil contain toxic pesticide residues, it also contains high levels of the chemical gossypol, which can interfere with spermatogenesis. In Nigeria, a randomized, controlled trial was designed to evaluate the effect of dietary aflatoxin on infertile men. Forty percent of the 50 infertile men in the study had aflatoxin in their semen samples, compared to eight percent of the fertile control group. In fertile men exposed to dietary aflatoxin had a 50-percent higher number of abnormal sperm than controls.
3. OLIGOSPERMIA.
The term oligospermia or oligozoospermia refer to semen with a low concentration of sperm and is a common finding in male infertility. Often semen with a decreased sperm concentration may also show significant abnormalities in sperm morphology and motility. Oligospermia can be as a result of many factors, some are permanent and some are reversible. Causes of oligospermia include an obstruction of the normal flow of sperm due to such conditions as testicular trauma and vasectomy. Oligospermia may also result from scarring due to surgery on the male reproductive system or from infection and sexually transmitted diseases. Treatment varies depending on the type and severity of oligospermia, the individual case, and the presence of complications. Treatment may include improving the diet, losing or gaining weight as needed, not smoking, reducing alcohol intake, and avoiding hot tubs and other factors that may create excessive heat around the testicles and reduce sperm count. Medications that may be used include vitamin E, vitamin C, antioxidants and hormone therapy.
4. TESTICULAR TRAUMA.
Blunt trauma to the scrotum may lead to intra testicular haematoma or even rupture of the testis; this causes damage of the testicular tissue and breach of the blood germinal epithelium barrier, causing production of antisperm antibodies.
5. ENVIRONMENTAL RISK FACTORS.
Current evidence suggests there may be environmental reasons for deteriorating sperm quality, including occupational exposure to various chemicals, heat, radiation, and heavy metals. In addition, exposure to environmental estrogens and pesticides has been linked to alterations in spermatogenesis. Lifestyle risk factors are also significant, including cigarette smoking, alcohol consumption, chronic stress, and nutritional deficiencies.
6. HEAVY METALS.
Another environmental concern with infertility is the toxic effects of heavy metals on sperm quality and production. In Hong Kong, infertile males were found to have approximately 40-percent higher hair mercury levels than fertile males of similar age. Occupational exposure to lead has been shown to cause a significant decrease in male fertility. Considering the occupational and environmental prevalence of heavy metals and their potentially negative interactions with the neuroendocrine system, a hair analysis should be included in the diagnostic work-up of idiopathic male infertility.
7. ESTROGENS AND PESTICIDES.
Increased exposure to estrogens is thought to be responsible for not only prenatal testicular damage, but may also contribute to post-natal depression of testicular function and spermatogenesis. Exogenous estrogens impact fetal development by inhibiting the development of Sertoli cells, which determine the lifelong capacity for sperm production. Circulating estrogens also inhibit enzymes involved in testosterone synthesis and may directly affect testosterone production. The synthetic estrogen, diethylstilbestrol (DES), is a well-documented example of this problem. DES was prescribed from 1945 to 1971 to millions of women during pregnancy. Male offspring from those women had a higher incidence of developmental problems of the reproductive tract, as well as diminished sperm volume and sperm count. Synthetic estrogens are still widely used in the livestock, poultry, and dairy industries. Men wishing to improve their fertility and sperm quality probably should avoid hormone-containing dairy products and meats and opt instead for organic or hormone-free foods. Many commonly-used pesticides, such as organochloride compounds, have estrogenic effects within the body. Chemicals such as dioxin, DDT, and PCBs are known to interfere with spermatogenesis. One study which examined the effect of DDT on male rat sexual development found low levels of DDT caused degeneration in sperm production, a decrease in the total number of sperm, and a reduced number of Leydig cells. The authors hypothesize that DDT acts as a hormonal disrupter, damaging the seminiferous epithelium and lowering local testosterone levels.
8. CIGARETTE SMOKING.
Cigarette smoking has been associated with decreased sperm count, alterations in motility, and an overall increase in the number of abnormal sperm. A study designed to evaluate seminal zinc levels in smokers and non-smokers found that although smokers did not have significantly lower zinc levels than non-smokers, seminal cadmium levels were significantly increased, especially in those smoking more than one pack per day. Experimental evidence also suggests nicotine can alter the function of the hypothalamic-pituitary axis, affecting growth hormone, cortisol, vasopressin, and oxytocin release, which then inhibits the release of luteinizing hormone (LH) and prolactin. Cigarette smokers were also shown to have higher levels of circulating estradiol and decreased levels of LH, follicle stimulating hormone (FSH), and prolactin than non-smokers, all of which potentially impact spermatogenesis. Smokers with low prolactin levels also demonstrated defects in sperm motility.
9. ANEJACULATION.
Primary anejaculation (anorgasmia) may occur as a result of psychosexual factors or neurological causes such as decreased sensitivity of the genital organs or high threshold of the ejaculatory reflex. Secondary anejaculation may occur following surgeries in the pelvis or abdomen that cause injury of the sympathetic chain, as in retroperitoneal lymph node dissection and panproctocolectomy. It may also occur in diabetic autonomic neuropathy and in other causes of autonomic neuropathy. Certain drugs such as antidepressants and alpha-blockers may also lead to anejaculation.
10. TESTICULAR TORSION.
If testicular torsion is not corrected within six hours, it leads to permanent damage and shrinking of the affected testis as a result of ischaemic necrosis. Moreover, this may be followed by production of antisperm antibodies, which affect the other healthy testis.
11. GENETIC CAUSES.
Structural and numerical chromosomal abnormalities are found in approximately per cent of infertile males and the prevalence may increase in men with complete absence of sperm. Genetic abnormalities include Y chromosome microdeletions, aneuploidy and chromosomal translocations. Klinefelter’s syndrome (XXY), the most common example of a numerical abnormality, occurs in 1:600 live male births and in up to 10 per cent of men with non-obstructive azoospermia. There are numerous other genes not yet identified that regulate sperm production, hormone production and hormone receptors. Any defect in such genes will impair fertility.