Preventable causes of male infertility by Prof Oladapo Ashiru OFR
Infertility is defined as a disease or disorder of the reproductive tract characterised by the inability to achieve a clinical pregnancy after one year of regular, unprotected sexual intercourse. For couples aged 35 years and above, it is the inability to obtain a clinical pregnancy after six months of regular, unprotected sexual intercourse.
Male infertility accounts for 40 per cent of the causes of infertility. Unlike the previous notion that infertility is a “female thing,” it is now clear that the male has an equal role to play during conception.
The causes of male infertility range from congenital and genetic causes to acquired causes and their different methods of management have been discovered and have kept improving throughout the years. We are also aware that the cornerstone to the management of any disease or disorder, including infertility, is prevention. Thus, this article focuses on the preventable causes of male infertility.
Human beings are exposed to numerous exogenous and environmental chemicals through various routes. There is a rapid expansion of chemical industries in both developed and developing countries, which have resulted in the release of xenobiotics into the environment. Most of them are airborne (which means they are inhaled into the respiratory system), while others can contaminate our water and food.
Whichever route humans get exposed to these factors, the male reproductive system is highly sensitive to them and they can cause infertility. Heavy metal is an example of such an environmental factor. Human beings could be exposed to heavy metals at small concentrations, usually through the intake of contaminated water and food or contact with contaminated air or soil.
Heavy metals, including lead, cadmium and mercury, could adversely affect the male reproductive system, either by causing a disruption in the hypothalamic-pituitary axis or by directly affecting spermatogenesis, which results in impaired semen quality.
Pesticidal toxicity affects several body organs, including the testis. Testicular weight, spermatogenesis, and semen parameters such as sperm motility and sperm count, are impacted. Sperm DNA damage and abnormal sperm morphology are also affected by organophosphorus.
Exposure to pesticides or crude oil during or before the preconception period can increase the risk of having an anencephalic child and, in the worst case, lead to fetal death from congenital anomalies.
Free radicals are generated from both endogenous and exogenous sources. Infection, excessive exercise, and mental stress are all responsible for endogenous free radical production. On the other hand, exogenous free radical production can occur as a result of exposure to environmental pollutants. They include exposure to heavy metals, certain drugs (cyclosporine, tacrolimus, gentamycin, and bleomycin), chemical solvents, and cooking (smoked meat, used oil, and fat). When these compounds penetrate the body, they degrade free radicals generated as by-products. The free radicals are responsible for several pathological conditions affecting the male (and even the female) reproductive system. They are one of the most important and preventable causes of male infertility.
Lifestyle factors are amendable habits and ways of life that can significantly influence overall health and well-being, including fertility. Some of these preventable lifestyle factors that have a direct influence on male fertility include excessive weight (obesity, whether central or peripheral obesity), smoking, alcohol consumption and recreational drugs. They have detrimental effects on sperm production.
Alcohol consumption can potentially contribute to congenital abnormalities, such as fetal alcohol syndrome and asthma in infants. Use of recreational drugs, such as methamphetamine, cocaine, and marijuana is associated with increased risk of a variety of congenital cardiac disabilities in children attributable to paternal use of these substances. Marijuana, containing the chemical 9-tetrahydrocannabinol may be directly toxic to the egg.
In this modern age where the use of a mobile phone is inevitable, it is essential to mention that a study conducted by Gorpinchenko in 2014 showed a positive correlation between mobile phone radiation exposure and sperm DNA-fragmentation level and decreased sperm motility. From this point of view, the habit of keeping a mobile phone in the trouser pocket or the duration of its use may have an impact on possible sperm generation.
Infections, such as chlamydia, gonorrhea, HIV and syphilis are common preventable STD’s that can harm the male urogenital tract. Their strains are known for their ability to immobilise and damage the morphology of spermatozoa by direct contact.
Microorganisms trigger a local inflammatory reaction, which then activates leukocytes and inflammatory mediators known to play essential roles in sperm DNA fragmentation. The inflammatory process in the genital tract may lead to a deterioration of spermatogenesis and obstruction of the seminal tract. These pathogens can also induce the production of sperm autoantibodies that fight the sperm cells. Mumps virus and Tb are other non-STD infections that can also affect the male reproductive system.
Infertility or significant alterations in semen parameters have been well documented in men taking Nitrofurantoin (antibiotics used in the treatment of bladder infections) and for patients on Sulfasalazine (used in the treatment of rheumatoid arthritis). Other commonly used medicines, such as Minocycline, are toxic to sperm at any concentration.
Until further information is available, clinicians must keep in mind that treatment with these antibiotics may adversely affect the fertility potential of men. Another recently discovered, little-known side effect of some antidepressants, such as Fluoxetine (Prozac), Sertraline (Zoloft) and Citalopram (Celexa) is their significant impact on men’s fertility.
These medications have been found to cut a man’s sperm count as well as the standard shape and motility of their sperm by 50 per cent. This effect can become evident in the first month after treatment and begins to have a significant impact after just three months taking them. Exogenous testosterone shuts down the Hypothalamic-Pituitary-Testicular axis, and suppress the intratesticular testosterone levels production to such a degree that spermatogenesis is drastically compromised and can lead to Azoospermia.