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In men, why do over 80% of sperm have abnormal form?


Here is the percentage of normal forms among fertile mens according to the centile (Source: Cooper et al. 2010):

  • 2.5: 3%
  • 5 (below this is Teratozoospermia): 4%
  • 10: 5.5%
  • 25: 9%
  • 50 (median): 15%
  • 75: 24.5%
  • 90: 36%
  • 95: 44%
  • 97.5: 48%

Men who have less than 4% of their sperm that have normal morphology are diagnosticated with Teratozoospermia (also called Teratospermia) and are likely to be infertile, though technically 5% of fertile men have Teratozoospermia.

I read on the internet that abnormally-shaped sperms are bad and useless because their abnormal shape prevents transport through the cervix and/or prevents them from adhering to the ovum.

But I think that if they were really that bad, Mother Nature would not have engineered the average men with 85% of their sperm abnormally-shaped.

And I also heard that even animals have a big fraction of their sperm that are abnormally-shaped.

So, in men, why do over 80% of sperm have abnormal form?


So I've dug a bit into how a 'normal morphological' form is defined and characterised, since assessing morphology into 'normal' and 'not normal' is always a very tricky thing.

Looking into the method section of the source you cited, we get:

All laboratories generating the data analysed here used standardized methods for semen analysis [… ] The various editions of the manual provided similar methods for assessing sperm concentration, motility and morphology but provided different criteria for categorising morphology.

So the problem begins already with the fact that there is not one, but multiple different recommended practices.
(For anyone interested the different staining methods used were: Bryan-Leishman [B], DiffQuik [D], Haematoxylin and Eosin [H], Papanicolaou [P], Quickdip [Q] and Shorr [S]. Of thses H, S and P were used for generation of the 'normal morphology' reference set).

Clearly this problem was also obvious to the authors, so they tried to restrict the data they used:

Although all centres reported using WHO procedures, the recommended methodologies have changed over time, and many centres have experienced difficulties with the subjective assessments of morphology. Data on normal sperm morphology were only included if results were reported as determined according to the so-called 'strict' (Tygerberg) method (WHO, 1992, 1999).

Fortunately these WHO guidelines are available on Google Books and they require the following points to met (most of which were defined by 95% confidence intervals of control samples):

  • head length 4.0-5.0µm
  • head width 2.5-3.5µm
  • head length-to-width ratio 1.5-1.75
  • well defined microsomal region compromising 40-70% of the head area
  • mid piece should be slender, <1µm
  • [mid piece should be] 1.5x size of the head
  • [mid piece should be] axially attached to the head
  • Cytoplasmic droplets should be less than half size of the head
  • Tail should be [… ] approximately 45µm long

Plus one very important sentence:

This classification scheme requires that all 'borderline' forms be considered abnormal

This sentence is important, because it means that each criterion stated has to be fulfilled for a single sperm to classified as morphological normal. If we take only the numeric requirements (which should cover ~95% of the normal value distribution for a healthy population) and assume that they are not correlated, this means that for any given single healthy sperm we have a $0.95^9 = 0.63 = 63\%$ chance that it is within the 95% interval of all defined parameters.
This means that applying this strict categorisation scheme should even for a 100% healthy population only result around 63% sperm cells categorised as morphologically normal (ignoring that the parameters are probably not interdependent which would make it a bit better).

If we now take into account that the analysed samples were probably not 100% healthy cells and remember that the (reported) difficulties of assessing morphology, I think that the reported values for 'morphological normal' are not as quite as unexpected as they might seem.

Note: all bold highlighting in the quote blocks was added by me.


Biological evolution occurs when there is a change in gene frequencies over time (as I recall). There are two components, or elements, required for this process:

  1. genetic variation, which provides the raw material
  2. natural selection, which results in the genes from the most successful reproducers being transferred to subsequent generations

The data you present support the hypothesis that “normal” sperm morphology in human males is not a strongly selected trait (because otherwise “normal” sperm would be more prevalent). Period. Full stop.

Any attempt to answer the “Why” part of this would have to be a conjecture, and ultimately untestable on an evolutionary scale.


Abnormal Sperm Morphology and Male Infertility

Abnormal sperm is a very severe problem and it is nothing like low sperm count or low motility of the sperm. Low sperm count can be corrected in more ways than one. Some of these ways are extremely simple such as wearing boxers instead of briefs and following a healthy lifestyle. Claim Your 20 Free Pregnancy Tests – Click Here

A few changes in day-to-day activities and diet can help you increase your sperm count. There is no doubt that some effort goes into treating low sperm count but when compared to abnormal sperm, it is a lot easier.

80% of the fertility problems related to males are concerned with low sperm count. Low sperm count is thus a major problem and lifestyle changes can get rid of it. A few lifestyle changes may also help improve the quality of male sperm.

Next comes low motility. Treating low motility is difficult when compared to low sperm count but not as difficult as treating abnormal sperm. Sometimes the only cure to this problem is fertility treatment. You may need to choose among the various treatments such as artificial insemination and in vitro fertilization.

Abnormal sperm is usually plenty in number and highly motile but since it is not of the normal physiology, it fails to fertilize the egg. It can reach the destination fallopian tube with ease because it has no problems with movement and survival but it can’t fertilize the egg. Such sperm is no worse than having no sperm at all.

It is important to know the reason behind abnormal sperm before looking into the treatment. Abnormal sperm may be due to internal conditions or external conditions. External conditions include unhealthy lifestyle, working in a harmful environment, and so on.

Internal conditions include kidney and liver disorders. Exposure to heat, radiations, any surgery, testicular failure, etc. are also causes of abnormal sperm. Another major cause is smoking. There is evidence that points to this.

Hence, if you smoke you should cease it immediately. It is important to be wary of all these, thus. More often than not it so happens that the cause is unknown and doctors simply can’t pinpoint the reason behind such abnormal sperm.

There are a few things that you can do in order to improve the quality of your sperm. You can take nutritional or herbal supplements such as ginseng, zinc, lycopene, vitamin C, and so on. You should include foods containing these in your diet.

You should also follow a healthy lifestyle. There is no guarantee that these will work but they are healthy foods and you must try them. Also, what may work for someone may not work for you. However, these don’t cost you much especially when compared to fertility treatments.

Thus it is a great idea to try these methods and see if your sperm quality improves. If not and you still can’t get pregnant, then you may wish to resort to fertility treatments, which are expensive and might work in your favor. Some of these include artificial insemination using a sperm donor and IVF using a sperm donor again.

Your doctor will be able to help you out with medication and the tests involved to find out the cause. Once you know the cause, it might be easier to eradicate the problem but as aforesaid, sometimes the reason is not known at all.


Out for the count: Why levels of sperm in men are falling

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If scientists from Mars were to study the human male's reproductive system they would probably conclude that he is destined for rapid extinction. Compared to other mammals, humans produce relatively low numbers of viable sperm – sperm capable of making that long competitive swim to penetrate an unfertilised egg.

As many as one in five healthy young men between the ages of 18 and 25 produce abnormal sperm counts. Even the sperm they do produce is often of poor quality. In fact only between 5 and 15 per cent of their sperm is, on average, good enough to be classed as "normal" under strict World Health Organisation rules – and these are young, healthy men. By contrast, more than 90 per cent of the sperm of a domestic bull or ram, or even laboratory rat, are normal.

Human males also suffer a disproportionately high incidence of reproductive problems, from congenital defects and undescended testes to cancer and impotency. As these also affect fertility, it's a minor miracle men are able to sire any children at all. In fact, an increasing number of men are finding themselves childless. Among the one in seven couples now classed as infertile, the "male factor" has been found to be the most commonly identified cause.

Next year marks the 20th anniversary of the WHO conference where a Danish scientist first alerted the world to the fact that Western men are suffering an infertility crisis. Professor Niels Skakkebaek of the University of Copenhagen presented data indicating sperm counts had fallen by about a half over the past 50 years. Sperm counts in the 1940s were typically well above 100m sperm cells per millilitre, but Professor Skakkebaek found they have dropped to an average of about 60m per ml. Other studies found that between 15 and 20 per cent of young men now find themselves with sperm counts of less than 20m per ml, which is technically defined as abnormal. In contrast, a dairy bull has a viable sperm count in the billions.

Experts in human reproductive biology were astonished by the Danish study. The declining trend seemed to indicate that men were on a path to becoming completely infertile within a few generations (although recent studies suggest the fall in sperm counts may have bottomed out). Professor Skakkebaek could offer no explanation for the trend other than to suggest that the fall may have something to do with the equally alarming rise in other reproductive disorders, such as cancer of the testes and cryptorchidism, the incomplete descent of the testes into the scrotum.

Experts began to talk of a new phenomenon affecting the human male, a collection of disorders known as testicular dysgenesis syndrome. They wanted to know what was causing it, because the changes were occurring too quickly to be a result of genetics. It must have something to with changing lifestyles or the environment of men, and almost everything was suggested, from exposure to chemical pollutants to the modern fashion for tight underpants. There is now an emerging consensus among some experts that whatever it is that is exacerbating the problems of male infertility, it probably starts in the womb. It is not the lifestyle of men that is problem, but that of their mothers.

The process of sperm production, called spermatogenesis, starts in adolescence, but the groundwork is laid down in the few months before and immediately after birth. An increasing number of studies point to a crucial "window" of testicular development that begins in the growing foetus and ends in the first six months of life. Interfere with this critical developmental period, and a baby boy will suffer the lifetime consequences of being a suboptimally fertile man.

So are we anywhere nearer to finding an explanation for why are so many more men today are suffering from reproductive problems?

"It's most likely a reflection of the fact that many environmental and lifestyle changes over the past 50 years are inherently detrimental to sperm production," says Professor Richard Sharpe, fertility research expert at the Medical Research Council. "It may be that different factors come together to have a combined effect." A number of studies point to a connection between early development in the womb and male reproductive problems in later life, especially low sperm counts. For example, men whose pregnant mothers were exposed to high levels of toxic dioxins as a result of the 1976 industrial accident in Seveso, Italy have been found to have lower-than-average sperm counts. But men exposed to dioxins in adulthood showed no such effect. Another study found women who ate large amounts of beef during pregnancy, a diet rich in potentially damaging chemicals called polycyclic aromatic hydrocarbons (PAHs), had sons with relatively low sperm counts. But eating beef as an adult man shows no similar impact.

Meanwhile, studies of migrants between Sweden and Finland, showed that a man's lifetime risk of testicular cancer tends to follow the country he was born in rather than the country where he was brought up. It was his mother's environment when she was pregnant with him, rather than his own as a boy or as an adolescent, that seems to have largely determined a man's risk of testicular cancer.

One of the strongest pieces of evidence in support of this idea comes from studies of people who smoke. A man who smokes typically reduces his sperm count by a modest 15 per cent or so, which is probably reversible if he quits. However, a man whose mother smoked during pregnancy has a fairly dramatic decrease in sperm counts of up to 40 per cent – which also tends to be irreversible.

Professor Sharpe said such findings can be explained by understanding how the first cells of the testes form. Sertoli cells, which in the adult act as guardians for the development of sperm cells, are the very first cells to form from a "genital ridge" of the human male foetus. The number of sperm that can be produced in an adult man is critically dependent on the number of Sertoli cells that develop in his foetus, so anything that interferes with the formation of Sertoli cells in a mother's womb will affect sperm production many years later. "Maternal-lifestyle factors in pregnancy can have quite substantial effects on sperm counts in sons in adulthood, and the most logical mechanism by which this could occur is via reducing the number of Sertoli cells," Professor Sharpe says.

But the key question now is to identify the relevant lifestyle and environmental factors.

This is proving tricky. Obesity, for instance, is a growing problem and it has been linked with reproductive problems in both men and women. One study has also indicated that overweight pregnant women tend to produce sons with poor semen quality. But is it being fat that is the cause, or the environmental chemicals stored in fat?

There has been a lot of interest in chemicals in the environment, especially those that can either mimic female sex hormones – oestrogenic chemicals – or block male sex hormones, specifically testosterone which plays a critical role in stimulating the development of Sertoli cells in the womb. So far, the Seveso study provides the clearest link between human foetal development, low sperm counts and prenatal exposure to an environmental chemical. But the dioxin concentrations from this industrial accident were exceptionally high.

It is more difficult trying to establish a similar, significant link between male reproductive problems and exposure to low concentrations of the many other environmental chemicals that may have weak oestrogenic or androgen-blocking properties, including substances as wide-ranging as pesticides, traffic fumes, plastics and even soya beans. Professor Sharpe says that much of the evidence to date is weak or non-existent.

"Public concern about the adverse effects of environmental chemicals on spermatogenesis in adult men are, in general, not supported by the available data for humans. Where adverse effects of environmental chemicals have been shown, they are usually in an occupational setting rather than applying to the general population," he says.

So although scientists are closing in on the critical window of foetal development in the womb that determines a man's fertility status in later life, they are still not sure about what it is that could be affecting this change in his reproductive status. But one thing is clear, it is his mother who almost certainly holds the key.


Infertility in men and women

Infertility happens when a couple cannot conceive after having regular unprotected sex.

It may be that one partner cannot contribute to conception, or that a woman is unable to carry a pregnancy to full term. It is often defined as not conceiving after 12 months of regular sexual intercourse without the use of birth control.

In the United States, around 10 percent of women aged 15 to 44 years are estimated to have difficulty conceiving or staying pregnant. Worldwide, 8 to 12 percent of couples experience fertility problems. Between 45 and 50 percent of cases are thought to stem from factors that affect the man.

Treatment is often available.

The following are common causes of infertility in men.

Semen and sperm

Share on Pinterest Sometimes the sperm cannot travel effectively to meet the egg.

Semen is the milky fluid that a man’s penis releases during orgasm. Semen consists of fluid and sperm. The fluid comes from the prostate gland, the seminal vesicle, and other sex glands.

The sperm is produced in the testicles.

When a man ejaculates and releases semen through the penis, the seminal fluid, or semen, helps transport the sperm toward the egg.

The following problems are possible:

  • Low sperm count: The man ejaculates a low number of sperm. A sperm count of under 15 million is considered low. Around one third of couples have difficulty conceiving due to a low sperm count.
  • Low sperm mobility (motility): The sperm cannot “swim” as well as they should to reach the egg.
  • Abnormal sperm: The sperm may have an unusual shape, making it harder to move and fertilize an egg.

If the sperm do not have the right shape, or they cannot travel rapidly and accurately towards the egg, conception may be difficult. Up to 2 percent of men are thought to have suboptimal sperm.

Abnormal semen may not be able to carry the sperm effectively.

  • A medical condition: This could be a testicular infection, cancer, or surgery.
  • Overheated testicles: Causes include an undescended testicle, a varicocele, or varicose vein in the scrotum, the use of saunas or hot tubs, wearing tight clothes, and working in hot environments.
  • Ejaculation disorders: If the ejaculatory ducts are blocked, semen may be ejaculated into the bladder
  • Hormonal imbalance: Hypogonadism, for example, can lead to a testosterone deficiency.
  • Genetic factors: A man should have an X and Y chromosome. If he has two X chromosomes and one Y chromosome, as in Klinefelter’s syndrome, the testicles will develop abnormally and there will be low testosterone and a low sperm count or no sperm.
  • Mumps: If this occurs after puberty, inflammation of the testicles may affect sperm production.
  • Hypospadias: The urethral opening is under the penis, instead of its tip. This abnormality is usually surgically corrected in infancy. If the correction is not done, it may be harder for the sperm to get to the female’s cervix. Hypospadias affects about 1 in every 500 newborn boys.
  • Cystic fibrosis: This is a chronic disease that results in the creation of a sticky mucus. This mucus mainly affects the lungs, but males may also have a missing or obstructed vas deferens. The vas deferens carries sperm from the epididymis to the ejaculatory duct and the urethra.
  • Radiation therapy: This can impair sperm production. The severity usually depends on how near to the testicles the radiation was aimed.
  • Some diseases: Conditions that are sometimes linked to lower fertility in males are anemia, Cushing’s syndrome, diabetes, and thyroid disease.

Some medications increase the risk of fertility problems in men.

  • Sulfasalazine: This anti-inflammatory drug can significantly lower a man’s sperm count. It is often prescribed for Crohn’s disease or rheumatoid arthritis. Sperm count often returns to normal after stopping the medication.
  • Anabolic steroids: Popular with bodybuilders and athletes, long-term use can seriously reduce sperm count and mobility.
  • Chemotherapy: Some types may significantly reduce sperm count.
  • Illegal drugs: Consumption of marijuana and cocaine can lower the sperm count.
  • Age: Male fertility starts to fall after 40 years.
  • Exposure to chemicals: Pesticides, for example, may increase the risk.
  • Excess alcohol consumption: This may lower male fertility. Moderate alcohol consumption has not been shown to lower fertility in most men, but it may affect those who already have a low sperm count.
  • Overweight or obesity: This may reduce the chance of conceiving.
  • Mental stress: Stress can be a factor, especially if it leads to reduced sexual activity.

Laboratory studies have suggested that long-term acetaminophen use during pregnancy may affect fertility in males by lowering testosterone production. Women are advised not to use the drug for more than one day.

Infertility in women can also have a range of causes.

Risk factors

Risk factors that increase the risk include:

  • Age: The ability to conceive starts to fall around the age of 32 years.
  • Smoking: Smoking significantly increases the risk of infertility in both men and women, and it may undermine the effects of fertility treatment. Smoking during pregnancy increases the chance of pregnancy loss. Passive smoking has also been linked to lower fertility.
  • Alcohol: Any amount of alcohol consumption can affect the chances of conceiving.
  • Being obese or overweight: This can increase the risk of infertility in women as well as men.
  • Eating disorders: If an eating disorder leads to serious weight loss, fertility problems may arise.
  • Diet: A lack of folic acid, iron, zinc, and vitamin B-12 can affect fertility. Women who are at risk, including those on a vegan diet, should ask the doctor about supplements.
  • Exercise: Both too much and too little exercise can lead to fertility problems. (STIs): Chlamydia can damage the fallopian tubes in a woman and cause inflammation in a man’s scrotum. Some other STIs may also cause infertility.
  • Exposure to some chemicals: Some pesticides, herbicides, metals, such as lead, and solvents have been linked to fertility problems in both men and women. A mouse study has suggested that ingredients in some household detergents may reduce fertility.
  • Mental stress: This may affect female ovulation and male sperm production and can lead to reduced sexual activity.

Medical conditions

Some medical conditions can affect fertility.

Ovulation disorders appear to be the most common cause of infertility in women.

Ovulation is the monthly release of an egg. The eggs may never be released or they may only be released in some cycles.

Ovulation disorders can be due to:

  • Premature ovarian failure: The ovaries stop working before the age of 40 years.
  • Polycystic ovary syndrome (PCOS): The ovaries function abnormally and ovulation may not occur.
  • Hyperprolactinemia: If prolactin levels are high, and the woman is not pregnant or breastfeeding, it may affect ovulation and fertility.
  • Poor egg quality: Eggs that are damaged or develop genetic abnormalities cannot sustain a pregnancy. The older a woman is, the higher the risk.
  • Thyroid problems: An overactive or underactive thyroid gland can lead to a hormonal imbalance.
  • Chronic conditions: These include AIDS or cancer.

Problems in the uterus or fallopian tubes can prevent the egg from traveling from the ovary to the uterus, or womb.

If the egg does not travel, it can be harder to conceive naturally.

  • Surgery: Pelvic surgery can sometimes cause scarring or damage to the fallopian tubes. Cervical surgery can sometimes cause scarring or shortening of the cervix. The cervix is the neck of the uterus.
  • Submucosal fibroids: Benign or non-cancerous tumors occur in the muscular wall of the uterus. They can interfere with implantation or block the fallopian tube, preventing sperm from fertilizing the egg. Large submucosal uterine fibroids may make the uterus’ cavity bigger, increasing the distance the sperm has to travel.
  • Endometriosis: Cells that normally occur within the lining of the uterus start growing elsewhere in the body.
  • Previous sterilization treatment: In women who have chosen to have their fallopian tubes blocked, the process can be reversed, but the chances of becoming fertile again are not high.

Medications, treatments, and drugs

Some drugs can affect fertility in a woman.

    (NSAIDs): Long-term use of aspirin or ibuprofen may make it harder to conceive.
  • Chemotherapy: Some chemotherapy drugs can result in ovarian failure. In some cases, this may be permanent.
  • Radiation therapy: If this is aimed near the reproductive organs, it can increase the risk of fertility problems.
  • Illegal drugs: Some women who use marijuana or cocaine may have fertility problems.

Cholesterol

One study has found that high cholesterol levels may have an impact on fertility in women.

Treatment will depend on many factors, including the age of the person who wishes to conceive, how long the infertility has lasted, personal preferences, and their general state of health.

Frequency of intercourse

The couple may be advised to have sexual intercourse more often around the time of ovulation. Sperm can survive inside the female for up to 5 days, while an egg can be fertilized for up to 1 day after ovulation. In theory, it is possible to conceive on any of these 6 days that occur before and during ovulation.

However, a survey has suggested that the 3 days most likely to offer a fertile window are the 2 days before ovulation plus the 1 day of ovulation.

Some suggest that the number of times a couple has intercourse should be reduced to increase sperm supply, but this is unlikely to make a difference.

Fertility treatments for men

Treatment will depend on the underlying cause of the infertility.

    or premature ejaculation: Medication, behavioral approaches, or both may help improve fertility.
  • Varicocele: Surgically removing a varicose vein in the scrotum may help.
  • Blockage of the ejaculatory duct: Sperm can be extracted directly from the testicles and injected into an egg in the laboratory.
  • Retrograde ejaculation: Sperm can be taken directly from the bladder and injected into an egg in the laboratory.
  • Surgery for epididymal blockage: A blocked epididymis can be surgically repaired. The epididymis is a coil-like structure in the testicles which helps store and transport sperm. If the epididymis is blocked, sperm may not be ejaculated properly.

Fertility treatments for women

Fertility drugs might be prescribed to regulate or induce ovulation.

  • Clomifene (Clomid, Serophene): This encourages ovulation in those who ovulate either irregularly or not at all, because of PCOS or another disorder. It makes the pituitary gland release more follicle-stimulating hormone (FSH) and luteinizing hormone (LH).
  • Metformin (Glucophage): If Clomifene is not effective, metformin may help women with PCOS, especially when linked to insulin resistance.
  • Human menopausal gonadotropin, or hMG (Repronex): This contains both FSH and LH. Patients who do not ovulate because of a fault in the pituitary gland may receive this drug as an injection.
  • Follicle-stimulating hormone (Gonal-F, Bravelle): This hormone is produced by the pituitary gland that controls estrogen production by the ovaries. It stimulates the ovaries to mature egg follicles.
  • Human chorionic gonadotropin (Ovidrel, Pregnyl): Used together with clomiphene, hMG, and FSH, this can stimulate the follicle to ovulate.
  • Gonadotropin-releasing hormone (Gn-RH) analogs: These can help women who ovulate too early—before the lead follicle is mature—during hmG treatment. It delivers a constant supply of Gn-RH to the pituitary gland, which alters the production of hormone, allowing the doctor to induce follicle growth with FSH.
  • Bromocriptine (Parlodel): This drug inhibits prolactin production. Prolactin stimulates milk production during breastfeeding. Outside pregnancy and lactation, women with high levels of prolactin may have irregular ovulation cycles and fertility problems.

Reducing the risk of multiple pregnancies

Injectable fertility drugs can sometimes result in multiple births, for example, twins or triplets. The chance of a multiple birth is lower with an oral fertility drug.

Careful monitoring during treatment and pregnancy can help reduce the risk of complications. The more fetuses there are, the higher the risk of premature labor.

If a woman needs an HCG injection to activate ovulation and ultrasound scans show that too many follicles have developed, it is possible to withhold the HCG injection. Couples may decide to go ahead regardless if the desire to become pregnant is very strong.

If too many embryos develop, one or more can be removed. Couples will have to consider the ethical and emotional aspects of this procedure.

Surgical procedures for women

If the fallopian tubes are blocked or scarred, surgical repair may make it easier for eggs to pass through.

Endometriosis may be treated through laparoscopic surgery. A small incision is made in the abdomen, and a thin, flexible microscope with a light at the end, called a laparoscope, is inserted through it. The surgeon can remove implants and scar tissue, and this may reduce pain and aid fertility.

Assisted conception

The following methods are currently available for assisted conception.

Intrauterine insemination (IUI): At the time of ovulation, a fine catheter is inserted through the cervix into the uterus to place a sperm sample directly into the uterus. The sperm is washed in a fluid and the best specimens are selected.

The woman may be given a low dose of ovary stimulating hormones.

IUI is more commonly done when the man has a low sperm count, decreased sperm motility, or when infertility does not have an identifiable cause. It can also help if a man has severe erectile dysfunction.

In-vitro fertilization (IVF): Sperm are placed with unfertilized eggs in a petri dish, where fertilization can take place. The embryo is then placed in the uterus to begin a pregnancy. Sometimes the embryo is frozen for future use.

Intracytoplasmic sperm injection (ICSI): A single sperm is injected into an egg to achieve fertilization during an IVF procedure. The likelihood of fertilization improves significantly for men with low sperm concentrations.

Sperm or egg donation: If necessary, sperm or eggs can be received from a donor. Fertility treatment with donor eggs is usually done using IVF.

Assisted hatching: The embryologist opens a small hole in the outer membrane of the embryo, known as the zona pellucid. The opening improves the ability of the embryo to implant into the uterine lining. This improves the chances that the embryo will implant at, or attach to, the wall of the uterus.

This may be used if IVF has not been effective, if there has been poor embryo growth rate, and if the woman is older. In some women, and especially with age, the membrane becomes harder. This can make it difficult for the embryo to implant.

Electric or vibratory stimulation to achieve ejaculation: Ejaculation is achieved with electric or vibratory stimulation. This can help a man who cannot ejaculate normally, for example, because of a spinal cord injury.

Surgical sperm aspiration: The sperm is removed from part of the male reproductive tract, such as the vas deferens, testicle, or epididymis.

Infertility can be primary or secondary.

Primary infertility is when a couple has not conceived after trying for at least 12 months without using birth control

Secondary infertility is when they have previously conceived but are no longer able to.


Discussion

The present opportunistic study of a convenience sample of men over the age of 50 years willing to provide semen samples but not for fertility evaluation shows that sperm concentration was not reduced by age, although semen volume was reduced by nearly 50% and total sperm output by 64%. In addition, sperm morphology and vitality were also more frequently pathological, especially involving sperm tail defects.

The strongest known determinants of semen volume are the positive relationship with time since last ejaculation ( Schwartz et al. , 1979 ) and the dependence of prostate and seminal vesicle fluid secretion on androgen exposure ( Kitahara et al. , 1998 Tash et al. , 2000 ). For practical reasons, the present study was unable to standardize the interval since last ejaculation, so the findings must be interpreted with caution. Anxiety associated with a scheduled prostate biopsy on the same day may have influenced ejaculate volume. Semen samples provided on the day of a vasectomy would be a valuable procedural control in this context, but such data were not available. Given the decreasing intercourse frequency with age ( Kinsey et al. , 1948 Feldman et al. , 2000 ), the apparently reduced semen volume with increasing age is more likely to reflect impaired androgen action, subclinical accessory gland pathology and/or ejaculatory defects (including treatment for prostate disorders) accumulating with age, rather than shorter abstinence intervals. Indeed, age-related reduction in ejaculation frequency may lead to underestimation of accessory gland hypofunction, whether androgen-dependent or not, in older men.

Sperm output, measured as total sperm per ejaculate, was substantially reduced in the older men, although the concomitant reduction in semen volume led to an apparent preservation of sperm density. This reduced sperm output with ageing is consistent with the impairment of spermatogenesis identified from detailed but small quantitative post mortem studies of sperm production rate (reviewed in Johnson, 1986 ), as well as a larger study of testis size ( Handelsman and Staraj, 1985 ) of men dying suddenly. These findings highlight the wisdom of considering total sperm output as a variable reflecting sperm production, at least in conjunction with sperm density.

Regarding sperm morphology, our sample of older men showed a decrease of proportions of normal sperm morphology and vitality. The aberrant sperm morphology in older men was most evident in defects of tail morphology, possibly reflecting the complex cellular structural assembly process of the axoneme providing more steps susceptible to age-dependent pathology. Such increasing proportion of defects may reflect degenerative changes with ageing in the germinal epithelium and/or in the intrinsic program directing spermiogenesis.

Only two previous studies have examined semen findings in substantial numbers of non-infertile men over 50 years of age. One study of 23 grandfathers over 60 years of age compared with 20 young fathers reported a non-significant 20% decrease in semen volume, a significant increase in sperm density, and no significant change in total sperm output or sperm morphology ( Nieschlag et al. , 1982 ). The small sample size of that study may have limited its power to detect changes in semen volume and sperm output. The lack of detailed morphological analysis according to ‘strict’ criteria as used in this study may also have led to an inability to detect minor defects in sperm morphology. Another study examined a healthy occupational cohort of 97 present or former non-smoking and generally healthy laboratory employees, including 42 men over the 50 years of age ( Eskenazi et al. , 2003 ). That study found a progressive decline in semen volume and total sperm output, while the sperm density demonstrated a non-significant downward trend, especially in men over 70 years of age. When compared with the WHO reference norms, the proportion with abnormal semen volume, sperm density and total sperm output all significantly increased progressively with age, with most striking effects over the age of 70 years. These findings are consistent with the present study, as well as with post mortem findings that demonstrated ageing effects on testis size were only significant in the eighth decade of life ( Handelsman and Staraj, 1985 ). The present study's findings are also consistent with the conclusions of a systematic literature review of ageing effects on semen analysis ( Kidd et al. , 2001 ). Following evaluation of 28 studies of semen analysis, it was concluded that ageing is associated with a decline in semen volume and sperm morphology, but not sperm density. However, that review did not evaluate total sperm output, a parameter less affected by abstinence interval, a variable in turn not well controlled in most studies. Furthermore, most studies reviewed comprised men attending fertility clinics, with very few over 50 years old. In that context the present study extends these findings to a larger group of older, non-infertile men.

The present opportunistic study suffers from the significant limitation of non-representative sampling that is virtually unavoidable in studies requiring semen analysis ( Cohn et al. , 2002 ). Similar issues essentially invalidate claims regarding historical changes in sperm output where non-representative samples were extrapolated to their epoch or geographical location ( Handelsman, 2001 ). It would be equally mistaken to extrapolate the present data to older men without strong caveats and independent replication. Nevertheless, by sacrificing sperm motility assessment, using this convenience sample we were still able to analyse ejaculate volume, sperm density, output, vitality and morphology in older men and compare with younger men recruited and examined in the same clinic and laboratory. However, the requirement for a semen sample will have limited the participation in the present study to not only potent men, but also to those with different attitudes, the impact or correlates of which on preservation of testicular function with ageing remains unknown.

An additional caveat on this sample is that the older men were biased by selection for requiring a prostate biopsy to evaluate possible prostate cancer. Prostate disease can theoretically obstruct the excurrent ductular system or have more general systemic effects on spermatogenesis. However, men with and without biopsy-proven prostate cancer did not differ with regard to semen variables. The general good health of the participants in this study together with the minimal extent and low grade of the biopsy-proven cancers make it unlikely that systemic effects of the cancer would be sufficient to influence sperm production. Although it is well established that chronic, even asymptomatic, disease may accelerate the age-dependent decline of blood testosterone ( Gray et al. , 1991a b Feldman et al. , 2002 ), spermatogenesis is relatively impervious to analogous influences such as exercise in young men ( Lucia et al. , 1996 ). These considerations suggest that sperm production and function in the older men was minimally or not influenced by their selection for prostate biopsy.

Evaluating the potential impact of ageing changes of this magnitude on fertility is speculative. It has long been known that conventional semen parameters overlap between men who are defined as fertile, infertile and the majority who, at any time, have undefined fertility. Repeated attempts to categorically distinguish such groups have generally been unsuccessful ( MacLeod and Gold, 1951 Meistrich and Brown, 1983 Guzick et al. , 2001 ). One approach is to compare the findings with a conventional benchmark, for which the WHO Semen Manual reference criteria would serve well. Although criticized for having an oracular rather than empirical basis, and for being set too high ( Handelsman, 1997 Lemcke et al. , 1997 Ombelet et al. , 1997 Chia et al. , 1998 Andersen et al. , 2000 ) or too low ( Bonde et al. , 1998 Zinaman et al. , 2000 ), the WHO criteria nevertheless represent a widely understood set of independent and conventional criteria for putatively normal semen finings for fertile men. By these criteria, the overall reduction in semen quality among the older men was modest and still largely conducive to fertility. Nevertheless, on average, men of this age may take longer to produce a pregnancy, and a higher proportion may warrant treatment for male infertility by conventional standards.

We conclude that in this convenience sample of older non-infertile men, sperm density is not reduced compared with younger men, but that reduced semen volume masks a decline in total sperm output. In addition, sperm morphology and vitality decline with age. Nevertheless these age-related declines are only modest in degree, and the extent to which they would increase delayed conception and treatment for male infertility remains uncertain. Considering the increasingly later age of marriage, the increasing frequency of remarriage and longer life expectancy of men who are theoretically capable of achieving paternity lifelong, the paucity of studies in this area is striking, and more detailed studies of non-infertile older men are desirable.

Statistical distribution of semen volume and sperm output in older and younger men

. Minimum . Q1 . Q2 . Q3 . Maximum . Mean . SD .
Older men ( n =55)
Age (years) 52 57 62 67 79 63 7
Prostate cancer 52 58 63 69 76 64 7
No prostate cancer 53 57 62 66 79 62 7
Semen volume (ml) 0.05 1 1.6 2.5 5 1.8 1.2
Prostate cancer 0.05 1 1.2 2.1 4 1.6 1.0
No prostate cancer 0.1 1 2 3 5 2.0 1.3
Sperm density (M/ml) 0 21 64 144 585 117 147
Prostate cancer 0 41 79 179 585 132 161
No prostate cancer 0 17 54 129 475 107 136
Total sperm (M/ejaculate) 0 27 95 * 282 1395 198 259
Prostate cancer 0 43 103 329 585 184 174
No prostate cancer 0 18 78 266 1395 210 322
Younger men ( n =409)
Age (years) 17 26 31 38 51 32 8
Semen volume (ml) 0.2 2 3 4.2 9.9 3.2 1.7
Sperm density (M/ml) 0 44 73 114 400 87 63
Total sperm (M/ejaculate) 0 114 203 368 2560 284 277
. Minimum . Q1 . Q2 . Q3 . Maximum . Mean . SD .
Older men ( n =55)
Age (years) 52 57 62 67 79 63 7
Prostate cancer 52 58 63 69 76 64 7
No prostate cancer 53 57 62 66 79 62 7
Semen volume (ml) 0.05 1 1.6 2.5 5 1.8 1.2
Prostate cancer 0.05 1 1.2 2.1 4 1.6 1.0
No prostate cancer 0.1 1 2 3 5 2.0 1.3
Sperm density (M/ml) 0 21 64 144 585 117 147
Prostate cancer 0 41 79 179 585 132 161
No prostate cancer 0 17 54 129 475 107 136
Total sperm (M/ejaculate) 0 27 95 * 282 1395 198 259
Prostate cancer 0 43 103 329 585 184 174
No prostate cancer 0 18 78 266 1395 210 322
Younger men ( n =409)
Age (years) 17 26 31 38 51 32 8
Semen volume (ml) 0.2 2 3 4.2 9.9 3.2 1.7
Sperm density (M/ml) 0 44 73 114 400 87 63
Total sperm (M/ejaculate) 0 114 203 368 2560 284 277

Tabulated is the range (minimum, maximum) of observed values and quartiles of distribution (Q2 is the median) of semen volume and sperm density and output. For each variable the first line is aggregate data with the data for men with and without histological prostate cancer on subsequent lines. There is no significant difference in sperm density ( P =0.12), but highly significant differences in semen volume ( P <10 −8 ) and total sperm output ( P <10 −5 ). All comparisons between men with and without histological prostate cancer on biopsy were not significant ( P >0.25) by the non-parametric Mann–Whitney test.

Statistical distribution of semen volume and sperm output in older and younger men

. Minimum . Q1 . Q2 . Q3 . Maximum . Mean . SD .
Older men ( n =55)
Age (years) 52 57 62 67 79 63 7
Prostate cancer 52 58 63 69 76 64 7
No prostate cancer 53 57 62 66 79 62 7
Semen volume (ml) 0.05 1 1.6 2.5 5 1.8 1.2
Prostate cancer 0.05 1 1.2 2.1 4 1.6 1.0
No prostate cancer 0.1 1 2 3 5 2.0 1.3
Sperm density (M/ml) 0 21 64 144 585 117 147
Prostate cancer 0 41 79 179 585 132 161
No prostate cancer 0 17 54 129 475 107 136
Total sperm (M/ejaculate) 0 27 95 * 282 1395 198 259
Prostate cancer 0 43 103 329 585 184 174
No prostate cancer 0 18 78 266 1395 210 322
Younger men ( n =409)
Age (years) 17 26 31 38 51 32 8
Semen volume (ml) 0.2 2 3 4.2 9.9 3.2 1.7
Sperm density (M/ml) 0 44 73 114 400 87 63
Total sperm (M/ejaculate) 0 114 203 368 2560 284 277
. Minimum . Q1 . Q2 . Q3 . Maximum . Mean . SD .
Older men ( n =55)
Age (years) 52 57 62 67 79 63 7
Prostate cancer 52 58 63 69 76 64 7
No prostate cancer 53 57 62 66 79 62 7
Semen volume (ml) 0.05 1 1.6 2.5 5 1.8 1.2
Prostate cancer 0.05 1 1.2 2.1 4 1.6 1.0
No prostate cancer 0.1 1 2 3 5 2.0 1.3
Sperm density (M/ml) 0 21 64 144 585 117 147
Prostate cancer 0 41 79 179 585 132 161
No prostate cancer 0 17 54 129 475 107 136
Total sperm (M/ejaculate) 0 27 95 * 282 1395 198 259
Prostate cancer 0 43 103 329 585 184 174
No prostate cancer 0 18 78 266 1395 210 322
Younger men ( n =409)
Age (years) 17 26 31 38 51 32 8
Semen volume (ml) 0.2 2 3 4.2 9.9 3.2 1.7
Sperm density (M/ml) 0 44 73 114 400 87 63
Total sperm (M/ejaculate) 0 114 203 368 2560 284 277

Tabulated is the range (minimum, maximum) of observed values and quartiles of distribution (Q2 is the median) of semen volume and sperm density and output. For each variable the first line is aggregate data with the data for men with and without histological prostate cancer on subsequent lines. There is no significant difference in sperm density ( P =0.12), but highly significant differences in semen volume ( P <10 −8 ) and total sperm output ( P <10 −5 ). All comparisons between men with and without histological prostate cancer on biopsy were not significant ( P >0.25) by the non-parametric Mann–Whitney test.

Statistical distribution of sperm morphology in older and younger men

. Minimum . Q1 . Q2 . Q3 . Maximum . Mean . SD .
Older men ( n =55)
Age (years) 52 57 62 67 79 63 7
% normal 0 6 15 19 40 14 9
Head 0 59 63 69 79 61 15
Neck 0 31 34 38 45 33 8
Tail 0 27 31 35 49 30 10
Cytoplasmic droplets 0 1 1 1 11 1.2 1.8
TZI 0 1.47 1.52 1.58 1.76 1.47 0.32
Vitality 0 37 54 69 85 51 22
Younger men ( n =84)
Age (years) 19 32 38 44 51 38 8
% normal 8 18 25 32 46 25 9
Head 42 57 63 72 89 63 11
Neck 18 27 31 37 54 32 8
Tail 0 9 16 22 35 16 9
Cytoplasmic droplets 0 0 0 1 7 0.5 1.2
TZI 1.26 1.44 1.48 1.53 1.66 1.48 0.08
Vitality 57 74 81 85 96 80 8
. Minimum . Q1 . Q2 . Q3 . Maximum . Mean . SD .
Older men ( n =55)
Age (years) 52 57 62 67 79 63 7
% normal 0 6 15 19 40 14 9
Head 0 59 63 69 79 61 15
Neck 0 31 34 38 45 33 8
Tail 0 27 31 35 49 30 10
Cytoplasmic droplets 0 1 1 1 11 1.2 1.8
TZI 0 1.47 1.52 1.58 1.76 1.47 0.32
Vitality 0 37 54 69 85 51 22
Younger men ( n =84)
Age (years) 19 32 38 44 51 38 8
% normal 8 18 25 32 46 25 9
Head 42 57 63 72 89 63 11
Neck 18 27 31 37 54 32 8
Tail 0 9 16 22 35 16 9
Cytoplasmic droplets 0 0 0 1 7 0.5 1.2
TZI 1.26 1.44 1.48 1.53 1.66 1.48 0.08
Vitality 57 74 81 85 96 80 8

Tabulated is the range (minimum, maximum) observed values and quartiles of distribution (Q2 is the median) of sperm morphology and vitality. There is highly significant difference for all variables ( P <0.0001 for all, except for TZI P =0.008) apart from neck and head pathology, which were not significantly different.

TZI = teratozoospermia index.

Statistical distribution of sperm morphology in older and younger men

. Minimum . Q1 . Q2 . Q3 . Maximum . Mean . SD .
Older men ( n =55)
Age (years) 52 57 62 67 79 63 7
% normal 0 6 15 19 40 14 9
Head 0 59 63 69 79 61 15
Neck 0 31 34 38 45 33 8
Tail 0 27 31 35 49 30 10
Cytoplasmic droplets 0 1 1 1 11 1.2 1.8
TZI 0 1.47 1.52 1.58 1.76 1.47 0.32
Vitality 0 37 54 69 85 51 22
Younger men ( n =84)
Age (years) 19 32 38 44 51 38 8
% normal 8 18 25 32 46 25 9
Head 42 57 63 72 89 63 11
Neck 18 27 31 37 54 32 8
Tail 0 9 16 22 35 16 9
Cytoplasmic droplets 0 0 0 1 7 0.5 1.2
TZI 1.26 1.44 1.48 1.53 1.66 1.48 0.08
Vitality 57 74 81 85 96 80 8
. Minimum . Q1 . Q2 . Q3 . Maximum . Mean . SD .
Older men ( n =55)
Age (years) 52 57 62 67 79 63 7
% normal 0 6 15 19 40 14 9
Head 0 59 63 69 79 61 15
Neck 0 31 34 38 45 33 8
Tail 0 27 31 35 49 30 10
Cytoplasmic droplets 0 1 1 1 11 1.2 1.8
TZI 0 1.47 1.52 1.58 1.76 1.47 0.32
Vitality 0 37 54 69 85 51 22
Younger men ( n =84)
Age (years) 19 32 38 44 51 38 8
% normal 8 18 25 32 46 25 9
Head 42 57 63 72 89 63 11
Neck 18 27 31 37 54 32 8
Tail 0 9 16 22 35 16 9
Cytoplasmic droplets 0 0 0 1 7 0.5 1.2
TZI 1.26 1.44 1.48 1.53 1.66 1.48 0.08
Vitality 57 74 81 85 96 80 8

Tabulated is the range (minimum, maximum) observed values and quartiles of distribution (Q2 is the median) of sperm morphology and vitality. There is highly significant difference for all variables ( P <0.0001 for all, except for TZI P =0.008) apart from neck and head pathology, which were not significantly different.


Treatment Options for BPH

Currently, the main options to address BPH are:

  • Watchful waiting
  • Medication
  • Surgery (prostatic urethral lift, transurethral resection of the prostate, photovaporization of the prostate, open prostatectomy)

If medications are ineffective in a man who is unable to withstand the rigors of surgery, urethral obstruction and incontinence may be managed by intermittent catheterization or an indwelling Foley catheter (which has an inflated balloon at the end to hold it in place in the bladder). The catheter can remain indefinitely (it is usually changed monthly).

Watchful Waiting

Because the progress and complications of BPH are unpredictable, a strategy of watchful waiting &mdash no immediate treatment is attempted &mdash is best for those with minimal symptoms that are not especially bothersome. Physician visits are needed about once per year to review the progress of symptoms, perform an examination and do a few simple laboratory tests. During watchful waiting, the man should avoid tranquilizers and over-the-counter cold and sinus remedies that contain decongestants. These drugs can worsen obstructive symptoms. Avoiding fluids at night may lessen nocturia.

Medication

Data is still being gathered on the benefits and possible adverse effects of long-term medical therapy. Currently, two types of drugs &mdash 5-alpha-reductase inhibitors and alpha-adrenergic blockers &mdash are used to treat BPH. Preliminary research suggests that these drugs improve symptoms in 30% to 60% of men, but it is not yet possible to predict who will respond to medical therapy or which drug will be better for an individual patient.

5-Alpha-Reductase Inhibitors

Finasteride (Proscar) blocks the conversion of testosterone to dihydrotestosterone, the major male sex hormone found in cells of the prostate. In some men, finasteride can relieve BPH symptoms, increase urinary flow rate and shrink the prostate, though it must be used indefinitely to prevent recurrence of symptoms, and it may take as long as six months to achieve maximum benefits.

In a study of its safety and effectiveness, two-thirds of the men taking finasteride experienced:

  • At least a 20% decrease in prostate size (only about half achieved this level of reduction by the one-year mark)
  • Improved urinary flow for about one-third of patients
  • Some relief of symptoms for two-thirds of patients

A study published last year suggests that finasteride may be best suited for men with relatively large prostate glands. An analysis of six studies found that finasteride only improved BPH symptoms in men with an initial prostate volume of over 40 cubic centimeters &mdash finasteride did not reduce symptoms in men with smaller glands. Since finasteride shrinks the prostate, men with smaller glands are probably less likely to respond to the drug because the urinary symptoms result from causes other than physical obstruction (for example, smooth muscle constriction). A recent study showed that over a four-year period of observation, finasteride treatment reduced the risk of developing urinary retention or requiring surgical treatment by 50%.

Finasteride use comes with some side effects. Impotence occurs in 3% to 4% of men taking the drug, and patients experience a 15% reduction in their sexual function scores regardless of their age and prostate size. Finasteride may also decrease the volume of ejaculate. Another adverse effect is gynecomastia (breast enlargement). A study from England found gynecomastia in 0.4% of patients taking the drug. About 80% of those who stop taking it have a partial or full remission of their breast enlargement. Because it is not clear that the drug causes gynecomastia or that it increases the risk of breast cancer, men taking finasteride are being carefully monitored until these issues are resolved. Men exposed to finasteride or dutasteride are also at risk of developing post-finasteride syndrome, which is characterized by a constellation of symptoms, including some that are sexual (reduced libido, ejaculatory dysfunction, erectile dysfunction), physical (gynecomastia, muscle weakness) and psychological (depression, anxiety, suicidal thoughts). These symptoms can persist long term despite discontinuation of finasteride.

Finasteride can lower PSA levels by about 50%, but it is not thought to limit the utility of PSA as a screening test for prostate cancer. The fall in PSA levels, and any adverse effects on sexual function, disappear when finasteride use is stopped.

To obtain the benefits of finasteride for BPH without compromising the detection of early prostate cancer, men should have a PSA test before starting finasteride treatment. Subsequent PSA values can then be compared to this baseline value. If a man is already on finasteride and no baseline PSA level was obtained, the results of a current PSA test should be multiplied by two to estimate the true PSA level. A fall in PSA of less than 50% after a year of finasteride treatment suggests either that the drug is not being taken or that prostate cancer might be present. Any increase in PSA levels while taking finasteride also raises the possibility of prostate cancer.

Alpha-Adrenergic Blockers

These drugs, originally used to treat high blood pressure, reduce the tension of smooth muscles in blood vessel walls and relax smooth muscle tissue in the prostate. As a result, daily use of an alpha-adrenergic drug may increase urinary flow and relieve symptoms of urinary frequency and nocturia. Some alpha-l-adrenergic drugs &mdash for example, doxazosin (Cardura), prazosin (Minipress), terazosin (Hytrin) and tamsulosin (selective alpha 1-A receptor blocker &mdash Flomax) &mdash have been used for this purpose. One recent study found that 10 milligrams (mg) of terazosin daily produced a 30% reduction of BPH symptoms in about two-thirds of the men taking the drug. Lower daily doses of terazosin (2 and 5 mg) did not produce as much benefit as the 10 mg dose. The report&rsquos authors recommended that physicians gradually increase the dose to 10 mg unless troublesome side effects occur. Possible side effects of alpha-adrenergic blockers are orthostatic hypotension (dizziness upon standing, due to a fall in blood pressure), fatigue and headaches. In this study, orthostatic hypotension was the most frequent side effect, and the authors noted that taking the daily dose in the evening can mitigate the problem. Another troubling side effect of alpha-blockers is the development of ejaculatory dysfunction (up to 16% of patients will experience this). In a study of over 2,000 BPH patients, a maximum of 10 mg of terazosin reduced average AUA Symptom Index scores from 20 to 12.4 over one year, compared to a drop from 20 to 16.3 in patients taking a placebo.

An advantage of alpha blockers, compared to finasteride, is that they work almost immediately. They also have the additional benefit of treating hypertension when it is present in BPH patients. However, whether terazosin is superior to finasteride may depend more on the prostate&rsquos size. When the two drugs were compared in a study published in The New England Journal of Medicine, terazosin appeared to produce greater improvement of BPH symptoms and urinary flow rate than finasteride. But this difference may have been due to the larger number of men in the study with small prostates, who would be more likely to have BPH symptoms from smooth muscle constriction rather than from physical obstruction by excess glandular tissue. Doxazosin was evaluated in three clinical studies of 337 men with BPH. Patients took either a placebo or 4 mg to 12 mg of doxazosin per day. The active drug reduced urinary symptoms by 40% more than the placebo, and it increased urinary peak flow by an average of 2.2 ml/s (compared to 0.9 ml/s for the placebo patients).

Despite the previously held belief that doxazosin was only effective for mild or moderate BPH, patients with severe symptoms experienced the greatest improvement. Side effects including dizziness, fatigue, hypotension (low blood pressure), headache and insomnia led to withdrawal from the study by 10% of those on the active drug and 4% of those taking the placebo. Among men treated for hypertension, the doses of anti-hypertension drugs may need to be adjusted due to the blood-pressure-lowering effects of an alpha-adrenergic blocker.

Phosphodiesterase-5 Inhibitors

Phosphodiesterase-5 inhibitors, such as Cialis, are commonly used for erectile dysfunction, but when used daily, they also can relax the smooth muscle of the prostate and overactivity of the bladder muscle. Studies examining the impact of daily Cialis use compared to placebo demonstrated a reduction in International Prostate Symptom Score by four to five points, and Cialis was superior to placebo in reducing urinary frequency, urgency and urinary incontinence episodes. Studies examining Cialis&rsquo impact on urine flow, however, have not shown meaningful change.

Surgery

Surgical treatment of the prostate involves displacement or removal of the obstructing adenoma of the prostate. Surgical therapies have historically been reserved for men who failed medical therapy and those who developed urinary retention secondary to BPH, recurrent urinary tract infections, bladder stones or bleeding from the prostate. However, a large number of men are poorly compliant with medical therapy due to side effects. Surgical therapy can be considered for these men to prevent long-term deterioration of bladder function.

Current surgical options include monopolar and bipolar transurethral resection of the prostate (TURP), robotic simple prostatectomy (retropubic, suprapubic and laparoscopic), transurethral incision of the prostate, bipolar transurethral vaporization of the prostate (TUVP), photoselective vaporization of the prostate (PVP), prostatic urethral lift (PUL), thermal ablation using transurethral microwave therapy (TUMT), water vapor thermal therapy, transurethral needle ablation (TUNA) of the prostate and enucleation using holmium (HoLEP) or thulium (ThuLEP) laser.

Thermal Treatments

Thermal procedures alleviate symptoms by using convective heat transfer from a radiofrequency generator. Transurethral needle ablation (TUNA) of the prostate uses low-energy radio waves, delivered by tiny needles at the tip of a catheter, to heat prostatic tissue. A six-month study of 12 men with BPH (age 56 to 76) found the treatment reduced AUA Symptom Index scores by 61%, and produced minor side effects (including mild pain or difficulty urinating for one to seven days in all the men). Retrograde ejaculation occurred in one patient. Another thermal treatment, transurethral microwave therapy (TUMT), is a minimally invasive alternative to surgery for patients with bladder outflow obstruction caused by BPH. Performed on an outpatient basis under local anesthesia, TUMT damages prostatic tissue by microwave energy (heat) that is emitted from a urethral catheter.

A new form of thermal therapy, called water vapor thermal therapy or Rezum, involves conversion of thermal energy into water vapor to cause cell death in the prostate. Studies examining the six-month prostate size after water vapor thermal therapy demonstrated a 29% reduction in prostate size by MRI.

With thermal therapies, several treatment sessions may be necessary, and most men need more treatment for BPH symptoms within five years after their initial thermal treatment.

Transurethral Incision of the Prostate (TUIP)

This procedure was first used in the U.S. in the early 1970s. Like transurethral resection of the prostate (TURP), it is done with an instrument that is passed through the urethra. But instead of removing excess tissue, the surgeon only makes one or two small cuts in the prostate with an electrical knife or laser, relieving pressure on the urethra. TUIP can only be done for men with smaller prostates. It takes less time than TURP, and it can be performed on an outpatient basis under local anesthesia in most cases. A lower incidence of retrograde ejaculation is one of its advantages.

Prostatic Urethral Lift (UroLift)

In contrast to the other therapies that ablate or resect prostate tissue, the prostatic urethral lift procedure involves placing UroLift implants into the prostate under direct visualization to compress the prostate lobes and unobstruct the prostatic urethra. The implants are placed using a needle that passes through the prostate to deliver a small metallic tab anchoring it to the prostate capsule. Once the capsular tab is placed, a suture connected to the capsular tab is tensioned and a second stainless steel tab is placed on the suture to lock it into place. The suture is severed.

Transurethral Prostatectomy (TURP)

This procedure is considered the &ldquogold standard&rdquo of BPH treatment &mdash the one against which other therapeutic measures are compared. It involves removal of the core of the prostate with a resectoscope &mdash an instrument passed through the urethra into the bladder. A wire attached to the resectoscope removes prostate tissue and seals blood vessels with an electric current. A catheter remains in place for one to three days, and a hospital stay of one or two days is generally required. TURP causes little or no pain, and full recovery can be expected by three weeks after surgery. In carefully selected cases (patients with medical problems and smaller prostates), TURP may be possible as an outpatient procedure.

Improvement after surgery is greatest in those with the worst symptoms. Marked improvement occurs in about 93% of men with severe symptoms and in about 80% of those with moderate symptoms. The mortality from TURP is very low (0.1%). However, impotence follows TURP in about 5% to 10% of men, and incontinence occurs in 2% to 4%.

Prostatectomy

Prostatectomy is a very common operation. About 200,000 of these procedures are carried out annually in the U.S. A prostatectomy for benign disease (BPH) involves removal of only the inner portion of the prostate (simple prostatectomy). This operation differs from a radical prostatectomy for cancer, in which all prostate tissue is removed. Simple prostatectomy offers the best and fastest chance to improve BPH symptoms, but it may not totally alleviate discomfort. For example, surgery may relieve the obstruction, but symptoms may persist due to bladder abnormalities.

Surgery causes the greatest number of long-term complications, including:

  • Impotence
  • Incontinence
  • Retrograde ejaculation (ejaculation of semen into the bladder rather than through the penis)
  • The need for a second operation (in 10% of patients after five years) due to continued prostate growth or a urethra stricture resulting from surgery

While retrograde ejaculation carries no risk, it may cause infertility and anxiety. The frequency of these complications depends on the type of surgery.

Surgery is delayed until any urinary tract infection is successfully treated and kidney function is stabilized (if urinary retention has resulted in kidney damage). Men taking aspirin should stop seven to 10 days before surgery, since aspirin interferes with blood&rsquos ability to clot.

Transfusions are required in about 6% of patients after TURP and 15% of patients after open prostatectomy.

Since the timing of prostate surgery is elective, men who may need a transfusion &mdash primarily those with a very large prostate, who are more likely to experience significant blood loss &mdash have the option of donating their own blood in advance, in case they need it during or after surgery. This option is referred to as an autologous blood transfusion.

Open Prostatectomy

An open prostatectomy is the operation of choice when the prostate is very large &mdash e.g., >80 grams (since transurethral surgery cannot be performed safely in these men). However, it carries a greater risk of life-threatening complications in men with serious cardiovascular disease, because the surgery is more extensive than TURP or TUIP.

In the past, open prostatectomies for BPH were carried out either through the perineum &mdash the area between the scrotum and the rectum (the procedure is called perineal prostatectomy) &mdash or through a lower abdominal incision. Perineal prostatectomy has largely been abandoned as a treatment for BPH due to the higher risk of injury to surrounding organs, but it is still used for prostate cancer. Two types of open prostatectomy for BPH &mdash suprapubic and retropubic &mdash employ an incision extending from below the umbilicus (navel) to the pubis. A suprapubic prostatectomy involves opening the bladder and removing the enlarged prostatic nodules through the bladder. In a retropubic prostatectomy, the bladder is pushed upward and the prostate tissue is removed without entering the bladder. In both types of operation, one catheter is placed in the bladder through the urethra, and another through an opening made in the lower abdominal wall. The catheters remain in place for three to seven days after surgery. The most common immediate postoperative complications are excessive bleeding and wound infection (usually superficial). Potential complications that are more serious include heart attack, pneumonia and pulmonary embolus (blood clot in the lungs). Breathing exercises, leg movements in bed and early ambulation are aimed at preventing these complications. The recovery period and hospital stay are longer than for transurethral prostate surgery.


Yes, it can. However, having higher amounts of abnormally shaped sperm has been associated with infertility in some studies. Usually, higher numbers of abnormally shaped sperm are associated with other irregularities of the semen such as low sperm count or motility. Men with abnormally shaped sperm may also have no trouble causing a pregnancy.

We don’t know. There’s no relationship between the shape of a sperm and its genetic material. Once the sperm enters the egg, fertilization has a good chance of taking place. However, as some of the abnormalities in sperm shape may be the result of genetic disturbances, there may be some male offspring who will inherit the same type of morphology abnormalities as are found in their fathers’ sperm morphology.


What causes a long liquefaction time?

Infection is the most common cause of a long liquefaction time. This is because of a few factors. First, whenever there is an infection in your body, there is a high amount of white blood cells present in the area to fight off the infection. The extra cells present can cause the natural break-down of proteins to slow even further as more cells have to be broken down. Check out this article for more info on the role of white blood cells in your fertility.
Second, this could indicate that your body is producing the correct amount of ingredients for healthy semen. Semen isn’t just comprised of sperm-in fact, sperm only make up roughly 5% of your semen. The rest is a mixture of nutrients for the sperm cells, acids, lipids, and the enzymes that will eventually cause liquefaction. These enzymes are produced by the prostate, so a long liquefaction time could also indicate an infection or dysfunction of your prostate. A visit to your doctor should be able to tell you if you have an infection. If one is found, antibiotic treatments will likely clear the infection, as well as the long liquefaction time associated with it.

Another cause of a long liquefaction time could be dehydration. It makes logical sense: semen is one of the bodily fluids that suffers when it can’t be replenished by water. If you’ve noticed that your semen has been thicker recently, try increasing your water consumption. To figure out how much water you should be drinking, take your weight in pounds and divide it by two: that’s how many ounces of water you should drink each day.


What Could Go Wrong?

Low motility numbers is referred to as asthenospermia. Asthenozoospermia can range from zero motile sperm to low numbers. The WHO defines asthenozoospermia as falling below 40% motility, but some prefer 20 million total motile count as a measure instead [1], [15].

In the general population, many men in Western countries suffer from suboptimal semen quality, as much as nearly 80% have some aspect of their semen analysis below optimal numbers [20]. It is not clear what percentage of that were due to low motility. However, by looking at subfertile or men diagnosed as infertile, we can see how low motility can impact fertility. 81.4% of one large population of men diagnosed with infertility have astenozoospermia [21].

Furthermore, your motility numbers and other semen parameters can all be normal but you might still have a problem with motility. The limitations of laboratory measurements means that there’s lots of factors missing when a technician analyzes your semen. Perhaps your sperm can’t survive the environment of your partner’s body, or your sperm have something wrong with their hyperactivation mechanism, the process where a sperm senses an egg nearby and goes into turbo-motility mode [22].


Molecular Bases of Cytoplasmic Male Sterility in Maize

C.S. LEVINGS III , D.R. PRING , in Physiological Genetics , 1979

VII SUMMARY

The male fertility system is unusual in that it results from the interaction of nuclear and cytoplasmic genes. This concept has developed from studies of the male sterile cytoplasms and their nuclear restorer genes. The cytoplasmic male steriles represent types which contain “mutations” of those cytogenes responsible for the male fertility trait. Especially pertinent is the fact that these cytoplasmic lesions can be corrected by nuclear genes, the Rf loci. This relationship implies the possibility that the same function may be coded in different genomes and that complementation may occur between the genetic systems, the nuclear and cytoplasmic. It further suggests that the cytoplasmic and nuclear genetic systems have evolved in concert with each other.

Evidence has been presented which indicates that the factors responsible for the cms trait are borne on the mitochondrial genome. Currently, the evidence is circumstantial, but it is persuasive because it has come from several different lines of investigation. The restriction enzyme fragment analyses of mtDNAs have consistently detected marked differences between normal and male sterile cytoplasms, while similar studies with ctDNAs have proved negative. The unusual organization of the mtDNA is in itself supportive. The large size of the mitochondrial genome and its apparent packaging among several molecules (molecular heterogeneity) gives it a realistic potential for contributing to the fertility trait. The S type of male sterility is a particular convincing example. In this case, the male sterility phenotype only occurs when the two unique DNAs (S–S and S–F) are present in the mitochondrion. When these unique DNAs are lost, the phenotype reverts to male fertility. Studies of the “target site” of the pathotoxin T have also implicated the mitochondrion. This indirect evidence is supportive of the contention that the cms trait is carried by the mitochondrial genome because of the absolute association found between the two traits, cms and disease susceptibility, in the T cytoplasm. Finally, differences have been found between the normal and cms types with respect to various mitochondrial proteins and enzymes. This then constitutes the evidence final proof awaits the mapping of mitochondrial genes which are responsible for male fertility and sterility.

Investigations of the S type of cms have revealed this system to be unstable. Mutations, both at the cytoplasmic and nuclear level, have been reported which have been explained on the basis of an episomal event. The presence of “fertility elements” which can be transposed between cytoplasmic and nuclear sites has been proposed. These elements may be the unique DNAs found associated with the mitochondrion from cms–S. If these elements can indeed be shown to be capable of transposition, it may be important in clarifying the origin of the cms systems.

The organization of the mitochondrial genome of maize is puzzling. Studies have indicated that the mitochondrion contain more than one class of DNA molecules. Although several explanations for the molecular heterogeneity phenomenon have merit, the exact cause remains unknown. Apparently, there is a relationship between the heterogeneity and the S type of cms. In this case, cms–S is associated with the presence in the mitochondrion of the two unique DNAs (S–S and S–F). It seems apparent that a clarification of the organization of the mitochondrial genome will be important in understanding the cms system.


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