Male infertility / Male Infertility Factors

Male Infertility

Its imperative to emphasize that male infertility is not one disorder but is a syndrome that results from one or more congenital or acquired conditions. With some exceptions most infertile men are healthy, have no symptoms and have few physical findings. However, infertility sometimes is the initial manifestation of a serious systemic illness. Most infertile men show oligozoospermia (reduced sperm count), asthenozoospermia (reduced motility), teratozoospermia (sperm with abnormal shape), hypospermia (reduced volume of the ejaculate) indicating that spermatogenesis is not only affected in quality but in quantity as well. A lower percentage of men show azoospermia (no sperm in the ejaculate), indicating no or very little sperm production or the presence of a mechanical obstruction that does not allow sperm to be present in the ejaculate even if spermatogenesis is not impaired.

Male infertility is a term applied when the male partner is identified to be the source of infertility. This is often diagnosed with one or more semen analysis. Abnormalities in one or more of the following components of the semen analysis may be one of the cause(s) of infertility: the amount of semen being ejaculated (low volume), low number of sperm (concentration, density or sperm count), low percentage of motile sperm (motility) and low percentage of normal sperm (morphology). The reasons for any one of the above listed conditions affecting the normalcy of the ejaculate may have different backgrounds.

The list is endless; however the most common may be genetic (cystic fibrosis), chromosomal abnormalities (Klinefelter’s syndrome), endocrine dysfunctions (at the brain or testicular level), tumors, conditions acquired after birth (fever, mumps, infections, and antibodies), etc. All of them result in one single symptom: lack of sufficient sperm to fertilize. Hopefully you realize now that the “lack of sufficient sperm to fertilize” cannot be easily treated considering the reduced pharmacological arsenal (drugs or hormones) available to treat male infertility. While drugs such as Clomid and FSH/LH, the most common pharmacological treatments in male infertility, may be effective to treat a reduced number of conditions afflicting infertile men, it may be totally counterproductive to use them on patients that do not need them. In some cases you may observe the “Paradoxical Effect”, which consists of making the condition worse than it was before treatment.

Considering all of the above, medical (drug) treatments are usually not recommended for male infertility primarily because of questionable effectiveness unless the condition is specifically diagnosed and the likelihood of response is high due to a logically applied treatment. Unfortunately, in most cases men with an abnormality in the semen analysis report tend to be treated with Clomid, FSH/LH or worse with supplements of dubious clinical effectiveness.

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The most deleterious effect of those “sperm booster” treatments may not be on their cost to the patient but on the time that couples spend trying to see an effect. Remember that the female is losing eggs every single day of her life, whether or not she is pregnant, sick or vacationing! In some cases, because of their age (> 35 years of age) women simply cannot wait any longer to see if a treatment on her partner is effective. The saddest situation may be when treatment on the male is finally effective but the spouse has no more eggs available in her ovaries because of the long time it took for the treatment to work. In other instances of male infertility, treatments may be effective but still the number of sperm necessary to induce a pregnancy may not be sufficient. But the treatment on him was 100% effective, right? I remember the case of a good friend of mine whose husband was azoospermia (no sperm in the ejaculate), after stuffing the poor guy with tons of herbal supplements, vitamins, Clomid, FSH/LH, and spiders hair, and many physicians later she found one on the internet. She was very impressed with his microsurgical skills and rates of success. Nearly all of his patients had successful surgeries. Against all advice, she decided to put her hopes and husband’s testis in this physician’s hands. Two years later she sent me an e-mail, understandably happy she was telling me that finally there were a few sperm in her husbands ejaculate. After another 24 months of waiting her husband’s sperm counts never rose above hundred thousand. This is 50-100 times lower than the minimum count required to achieve a pregnancy via intercourse or intrauterine insemination. However, the surgical procedure was effective but not enough to achieve a pregnancy, the final objective of theirs efforts. About 6 years later, thousands of dollars wasted, and countless hours of emotional stress she was finally able to conceive with intrauterine insemination using donor sperm. Now they are the happy parents of a precious baby.

In summary, pharmacological treatment may be effective in some selected cases of male infertility. However, it should be judiciously applied to those who clinically may respond to it. Pharmacological treatment is not for everybody and in some cases it may cause more harm than good. Treatment to improve the male condition may not be effective but technologies are available to help you and your partner to achieve a pregnancy. Sperm preparations for intrauterine inseminations, or IVF/ICSI coupled with ejaculated or surgical sperm retrieval may be the answer to help you conquer infertility.

Pathologic conditions

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Genetic and chromosomal conditions. After the clinical application of ICSI to treat severe cases of male infertility it has been more recognized the role of genetic causes of infertility. Genes and clusters of genes localized in the “Y” chromosome have been associated with normal spermatogenic functions. The “Y Chromosome deletion” test is a test designed to determine the integrity of the Y chromosome. Deletions of some or all genes responsible for spermatogenesis may result in impaired sperm production. Some other genes have been associated with mutations that result in oligozoospermia (low counts) and asthenozoospermia (poor motility) such is the case of the POLG mutant gene that has recently been associated with patients displaying poor motility and concentration. This field is constantly changing and is likely that most of the abnormalities observed in a semen analysis would be linked to genetic abnormalities.

Primary testicular failure

The testicular tissue may be the main cause of infertility. Recognized in adult men by the finding of increased circulating blood FSH and LH levels. Indicating that the gonad steroids (testosterone and estradiol) and to some extent inhibin are not being produced at the testicular level and therefore do not cause a negative feedback on the hypothalamus to reduce FSH and LH in blood. Congenital disorders that cause primary testicular failure are: Klinefelter’s syndrome, XYY male, cryptorchidism, vanishing testis syndrome, Noonan’s syndrome, myotonic muscular dystrophy and sickle cell disease. Acquired disorders that result in primary testicular failure are: mumps, trauma to the testis, testicular tumors, torsion, varicocele, spinal cord injury, liver and kidney disease, drugs, irradiation, aging.

Hypogonadotropic hypogonadism

This is testicular dysfunction due to insufficient stimulation of the testis by brain released FHS/LH. Most men with this condition have low testosterone levels and LH levels are in the low to low-normal range. Among the disorders that produce this condition are: Congenital disorders. Kallaman’s, Prader-Willis and fertile eunuch syndromes. Acquired: pituitary tumors, head trauma, meningitis, irradiation, liver and renal disease, stress, etc…

Other environmental causes of infertility

Drugs and toxins. They exert their effects at different levels of the reproductive tract. For example diethylstilbestrol and ant androgens act when the fetus is in the uterine cavity. Occupational exposure agents such as lead, estrogens, insecticides, herbicides, radiations, etc; Prescription drugs associated with reproductive dysfunction such as chemotherapeutic agents, and androgens; Drugs that alter male sexual function: Testosterone biosynthesis inhibitors (Spironolactone, ketoconazole, cyproterone acetate), androgen antagonists (flutamide, cimetidine), inhibitors of erectile function, ejaculation or fertilization (antihypertensives, neuroleptics, antidepressants), and recreational illicit drugs (ethanol, marihuana, cocaine, cigarettes).

Ejaculatory dysfunctions. Retrograde ejaculation and failure of ejaculation are rare events in infertile men. Diabetes mellitus is the most common cause of retrograde ejaculation. Retrograde ejaculation may be pharmacologically treated and or sperm may be collected from the bladder after dietary supplements are taken to change the urine pH.

Testicular function is normal in men with diabetes. Some drugs (narcotics, sedatives, psychotropics and antiadrenergics) may inhibit ejaculation. Other causes such as operations on the pelvic area (prostatectomy) may result in erectile dysfunction also.

Genital tract obstructions. Occur in 3-13% of infertile men. Obstructive azoospermia occurs in patients with reproductive tract infections of bacterial origin, trauma or disorders that involve mucociliary transport diseases that result in bronchitis and bronchiectasis. Also azoospermia occurs in patients with congenital absence of the vas deferens a condition that results on some patients with cystic fibrosis.

PAINTING AND DECORATING MAY BE HARMFUL TO MALE FERTILITY

New research shows that the sperm of men who work as painters and decorators is likely to be of poorer quality. This is due to their exposure to chemical solvents known as glycol ethers in water-based paints and other substances used in their trade. The scientists, from the universities of Sheffield and Manchester in the UK, published their findings in the BMJ journal of Occupational Environmental Medicine. The researchers examined the working lives of 2,118 men across the UK in an attempt to assess how environmental work factors, particularly exposure to chemical substances, affected male fertility. The research took place in 14 fertility clinics in 11 cities across the UK.

The research showed that men working with glycol ethers have a 2.5-fold increased risk of having high numbers of sperm with low motility (swimming ability) compared to men who are not often exposed to the chemicals. Sperm motility is an important factor in the fertility of men and the concentration of motile sperm per ejaculate has shown to bear direct relevance to the chances of conception. As well as this, a sperm’s morphology (its size and shape) and the quality the DNA contained in it are also important factors that may be affected by chemical exposure. However, the researchers also concluded that, aside from glycol ethers, there are few other common chemical threats to male fertility in the workplace.

The study also looked at other non-chemical factors in the men’s lifestyles that may have an effect on their fertility. The researchers discovered that men who had undergone previous testicular surgery or who undertook manual work were more likely to have lower numbers of motile sperm, whereas men who drank alcohol regularly or wore boxer shorts were more likely to have better semen quality.

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Other agents that affect male fertility

Agent / Medication

Gonado-toxic

Altered HPG Axis

Decreased Libido

Erectile Dysfunction

Fertilization Potential

Recreational/Illicit

Alcohol
Cigarettes
Marihuana
Opiates
Cocaine

 

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Antihypertensives

Thiazide Diuretics
Spironolactone
β-blockers
Ca++ Channel Blockers
Α-Adrenergic Blockers

 





 


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Psychotherapeutic

Antipsychotics
Tricyclic

Antidepres.
MAOIs
Phenotiazines
Lithium

 





 

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Chemotherapeutic

Alkylating Agents
Antimetabolites
Vinca Alkaloids

 

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Hormones

Anabolic Steroids
Testosterone
Antiandrogens
Progest. Derivatives
Estrogens

 




 

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Antibiotics

Nitrofurantoin
Erythromycin
Tetracyclines
Gentamycin

 

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Miscelaneous

Cimetidine
Cyclosporine
Colchicine
Allopurinol
Sulfasalazine

 





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Hypothalamic-pituitary-gonad (HPG), Monoamine Oxidase Inhibitors (MAOIs),
Nudell, et al., Urol. Clin. North Am. 2002 (29): 965-973.“““`

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