Male Sexuality

Almost all laboratories will conduct tests and report on the following information using values established by the World Health Association.
* Concentration (sometimes referred to as the “count”): This is a measurement of how many million sperm there are in each milliliter of fluid. There are various techniques for obtaining this number - some prove to be more accurate than others. Average sperm concentration is more than 60 million per milliliter (>60 million/cc). Counts of less than 20 million per milliliter (<20 million/cc) are considered sub-fertile.
* Motility (sometimes referred to as the “mobility”): This describes the percentage of sperm which are moving. 50% or more of the sperm should be moving. This number can increase in cases of  male enhancement.
* Morphology: This describes the shape of the sperm. The sperm are examined under a microscope and must meet specific sets of criteria for several sperm characteristics in order to be considered normal. Most commercial laboratories will report WHO morphology (i.e. use World Health Organization criterion). 30% of the sperm should be normal by these criteria.

* Volume: This is a measurement of the volume of the ejaculate. Normal is 2 milliliters (2 ccs) or greater. The volume may be low if a man is anxious when producing a specimen, if all of the specimen is not caught in the collection container, or if there are hormonal abnormalities or ductal blockages.

* Total Motile Count: This is the number of moving sperm in the entire ejaculate. It is calculated by multiplying the volume (cc) by the concentration (million sperm/cc) by the motility (% moving). There should be more than 40 million motile sperm in the ejaculate.

* Standard Semen Fluid Tests: Color, viscosity (how thick the semen is) and the time until the specimen liquefies should also be measured. Abnormalities in the seminal fluid may adversely affect the sperm. For example, if the semen is very thick it may be difficult for the sperm to move through it and into the woman’s reproductive tract.

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Although the frequency of erectile dysfunction increases with advancing age, societal attitudes have discouraged older men from seeking treatment. Interest in sex was considered appropriate for young men only; the “dirty old man” was an object of derision.

While physicians now recognize sexuality as a legitimate concern for men regardless of their age, as a gerontologist, I often encounter men in their 70s or 80s who are embarrassed to bring up the subject. (Those who are in a longstanding marriage may be more willing to mention it than those who are trying to start a new relationship.) Yet, as Wierman’s case histories illustrate, when patients do come forward, the physician often can provide effective treatment not only for the erectile dysfunction itself, but also for underlying disorders.

The disorders I see most often in my practice are endocrine, particularly thyroid disease. Both hyperthyroidism and hypothyroidism can cause erectile dysfunction as well as subtle problems such as confusion, depression, sleep disruption, and weight loss or gain. All of these symptoms could be written off as “just old age”–but as with many other complaints in the elderly, that is not an acceptable answer. The patient whose physician says “It’s just your age” should seek a second opinion.

I have had several patients who presented with impotence as their chief complaint–sometimes their only complaint–who proved to have hypothyroidism. Moreover, there is a syndrome among the elderly called apathetic hyperthyroidism, which stands in strong contrast to the hyperactivity, insomnia, and jitteriness seen in the typical young patient with hyperthyroidism.

Indeed, because thyroid disorders occur so commonly with age–affecting perhaps 10% of the elderly population–I order a thyroid panel almost routinely whenever I see a new patient. Thyroid function often is abnormal, and correcting it makes the patient feel and function better in many dimensions, including sexuality.

I would also underscore Wierman’s point that drug side effects are an important cause of erectile dysfunction. Antihypertensive agents, as in the second case, are a frequent offender, but many other drugs–and many drug interactions–can cause impotence or loss of libido. In geriatric medicine, it is standard practice to review every single one of a patient’s medications and its potential side effects to make sure that the complaint is not drug-related. That practice also applies in erectile dysfunction, especially since the advent of sildenafil. Indeed, I worry that some patients may be receiving sildenafil as a treatment for erectile dysfunction that is in fact the result of another medication that the patient is taking. In general, it is a bad idea to prescribe a new medication in order to counteract the side effect of a current medication. Instead, the physician should try to carefully withdraw the offending medication and then substitute a different class of drug.

Circumspection is especially important with a newly released drug such as sildenafil. Although relatively few side effects of this drug have been reported, a complete understanding of the side-effects of any new drug cannot be established until it has been used by a large number of patients for an extended period. Even if sildenafil turns out to have no as yet unknown side effects, those currently reported (e. g., decreased blood pressure) may cause adverse interactions with other medications. Wierman’s caution about that possibility is well taken.

The case of the diabetic patient provides an excellent example of what we hope to prevent with the new emphasis on tight control of blood glucose levels in patients with this disease. It had always been assumed that diabetes leads more or less inexorably to neuropathy and vasculopathy and their resulting dismal array of complications, including impotence. Recent studies have shown, however, that very tight blood glucose control can slow or even halt the progression of diabetic complications.

While erectile function was not used as an outcome measure in those studies, pathophysiology and common sense argue that because tight blood glucose control prevents other neurologic and vascular complications, it will also prevent erectile dysfunction. I would not hesitate to use that argument as a motivational tool in a diabetic patient.

Finally, I would reinforce Wierman’s observation about the psychological component in all men with erectile dysfunction. Physicians need to be more willing to talk with patients about this issue, or–if they do not wish to talk about it themselves–to set up a clear and easy system of referral to a skilled counselor. If the psychologic component can be addressed, then even a slight improvement in the physiologic component may be all it takes to restore erectile function.

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Recent advances in our knowledge of the physiology of erection have facilitated understanding of the pharmacodynamics of sildenafil. Erection is initiated by dilation of the arterial bed, which increases blood flow and pressure; it is maintained by restriction of venous outflow. Previously it was believed that the parasympathetic system was critical in maintaining erection. Now we know that the major player is the nonadrenergic, noncholinergic (NA-NC) system, which was identified 50 years ago but never studied in detail until recently. The NA-NC system uses nitric oxide as a neurotransmitter. Through its second messenger, cyclic guanine monophosphate (cGMP), nitric oxide triggers relaxation of penile endothelium and smooth muscle, allowing expansion of the lacunar spaces within the corpora and the trapping of blood by compression of peripheral draining venules.

Sildenafil, a type 5 phosphodiesterase inhibitor, prevents the breakdown of cGMP, thus prolonging erection. It has no effect on libido and it does not cause erection, but it maintains an erection once it has been achieved. Although the NA-NC system is particularly prominent in the penis, it is also found in the heart, the brain, and other organs. Its presence in the eye explains the blue visual hue that some patients experience after taking sildenafil.

The most common side effects of sildenafil are headache, flushing, and dyspepsia. It can also decrease blood pressure. Because the decrease may be synergistic with the hypotensive action of nitrates, sildenafil is contraindicated in patients taking a medication that contains nitrates, such as nitroglycerin.

In addition, sildenafil alters the half-life of many other medications, and many medications change the half-life of sildenafil. The list of agents that can interact with sildenafil includes such common medications as nonselective beta-blockers, erythromycin, itraconazole, potassium-sparing diuretics, and cimetidine. It is not known whether those interactions affect the side effects of sildenafil–especially the incidence or severity of hypotension. In initial clinical trials, hypotension was reported in about 3% of patients, but those trials included a large percentage of young men with psychogenic impotence. Obviously, patients with vascular disease or diabetes have more problems with blood pressure regulation and theoretically with orthostatic hypotension. A number of deaths have occurred among patients taking sildenafil since it became available. The U. S. Food and Drug Administration (FDA) is currently investigating those deaths.

Evaluating sildenafil has been difficult because it is one of several drugs that have been approved during the past two years through a new FDA process. Previously, a drug was not approved until studies had been published. Now the FDA allows pharmaceutical companies to submit unpublished studies. With this streamlined process, a drug can be approved before clinicians have the chance to read peer-reviewed data and decide whether their patients falls into the same category as patients in the initial studies. Instead, the physician has only the drug company brochure, which does not offer the detail of a peer-reviewed journal article.

The first study of data on different patient populations taking sildenafil was published several months after the drug became available for clinical use. While the package insert indicated an overall efficacy of 82% (vs 24% for placebo), analysis showed that the efficacy was 68% in patients with hypertension, 57% in diabetes, 61% after trans-urethral prostatic resection, and 43% after radical prostatectomy. Moreover, those results were obtained in a selected patient population, not from general clinical use.

Physicians need additional information from peer-reviewed studies so that they can assess the risk-benefit ratio of sildenafil and make rational treatment decisions in individual cases. Meanwhile, third-party payers are trying to decide whether they should reimburse the cost of the drug. Arguments against coverage include the fact that erectile dysfunction is not a life-threatening condition. Also, since many third-party payers do not pay for oral contraceptives for women, they feel that they should not reimburse for a drug that enhances sexual performance in men.

In any case, newspaper reports indicate that sales of sildenafil have slowed in recent months. The decrease has been attributed to refusals for insurance coverage and increasing reports of side effects. A human element may also be involved. For example, in several studies of penile prostheses, patient interviews confirmed that the prostheses functioned well, but interviews with the patients’ wives revealed that the patients were not using it. Similar findings have been reported in studies of other treatments for erectile dysfunction; the actual frequency of use is much less than that initially described by the patient. The ability to have sex is only one element in a complicated equation that determines whether or how often a patient has sexual relations.

Future Possibilities. Other oral agents for erectile dysfunction are undergoing clinical trials and should soon be available. Apomorphine, an opiate antagonist, has shown up to 70% efficacy in patients with psychogenic impotence; it will probably be available for clinical use late this year. Also under FDA review is an oral preparation of phentolamine. This agent blocks norepinephrine, causing smooth-muscle relaxation and vasodilation. In preliminary studies, it was effective in 60% to 80% of patients and had fewer side effects than sildenafil.

For patients using intracavernosal injection, a combination of vasoactive intestinal peptide (VIP) and phentolamine is under investigation. Both agents are smooth muscle relaxants, and vasoactive intestinal peptide appears to increase production of nitric oxide.

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A 58-year-old man complained of loss of libido and erectile dysfunction. Pubertal development had been normal, as had sexual function until about two years ago. Since then, he had noted a gradual decline in his ability to achieve and maintain an erection. The patient was otherwise in good health and taking no medications.

On review of systems, the patient noted a history of frontal, throbbing headaches that he attributed to job-related stress. During the past six months, he had also noted some trouble with his vision. On additional questioning, he said that he did not need to shave as frequently as in the past, was experiencing fatigue and occasional hot flashes, had dry skin, had gained 10 lb during the past year, and was constipated. In addition to stress at work, he expressed concern about his relationship with his girlfriend.

This patient’s erectile dysfunction appears to be largely hormonal in origin. The causes of erectile dysfunction fall into five categories: vascular, neurogenic, hormonal, iatrogenic (i.e., caused by medication), and psychogenic. Typically, more than one cause is involved, and regardless of the precipitating factor, by the time the patient presents to a physician, there is also a psychogenic component.

A directed history is critical for distinguishing the different categories of erectile dysfunction. Historically, men with erectile dysfunction have not talked to their physicians about it, and physicians have not felt comfortable asking about it. While that reticence may be diminishing–in part owing to awareness of new treatment options–patients still rarely volunteer sufficient information.

The first step in the history is to determine the scope of the problem. Similar research is needed when male enhancement or penis enhancement is sought. Erectile dysfunction is defined as the consistent inability to attain and maintain penile erection sufficient to permit satisfactory sexual intercourse. That definition comprises a spectrum of possibilities: Does the patient have no erections at all? No morning erections? Does he have erections, but only partial ones? Although the degree of dysfunction does not correlate with the underlying cause, establishing a baseline of function is valuable for gauging the effect of therapy. Onset of the dysfunction does have diagnostic significance, however: gradual onset suggests a physiologic cause; psychogenic impotence typically–although not invariably–has an acute onset.

To narrow the differential diagnosis, physicians must be specific in their questioning, not only about erectile dysfunction but about other signs and symptoms. In this case, the patient had experienced both loss of libido and erectile dysfunction. Loss of the two functions can occur separately in men, although libido and sexual function usually are not separated in women. The mechanisms that control libido are not clearly understood, but it is known that decreased libido tends to be associated with hormonal deficits. One exception is psych-iatric medications; they can decrease libido without affecting erectile function.

This patient’s normal puberty suggests that maturation of the hypothalamic-pituitary-gonadal axis was normal. However, shaving less frequently and occasional hot flashes strongly suggest decreased androgen production. Just as women have hot flashes when their estrogen levels fall during menopause, men whose androgen levels are falling to prepubertal levels also experience hot flashes.

The history of headaches and the recent onset of visual problems are important clues–clues that too often are ignored in such cases. They suggest a space-occupying lesion of the hypothalamus or pituitary. Fatigue, weight gain, constipation, and dry skin are all nonspecific symptoms, but when added to the rest of the clinical picture, they suggest another pituitary deficiency: hypothyroidism caused by abnormal thyroid-stimulating hormone (TSH) secretion. Because thyroid dysfunction can cause erectile dysfunction, thyroid testing is indicated whenever there is a possibility of hypothyroidism, especially in an older patient. Although thyroid abnormalities are less common in men than in women, about 3% to 4% of men over age 60 have autoimmune thyroid disease.

Although it is unlikely, psychological stress cannot yet be ruled out as a cause of erectile dysfunction is this patient. He is under stress at work, is having problems with his relationship, and is undoubtedly suffering performance anxiety because of his erectile dysfunction.

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Case 1 Treatment
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The patient was treated with cortisol and thyroid hormone, after which transsphenoidal pituitary surgery was performed and the tumor resected. Histopathologic analysis confirmed that the tumor was a glycoprotein-secreting adenoma.

Several weeks after surgery, the patient reported that his libido and erections had returned. Six weeks postoperatively, hormonal therapy was withdrawn. Subsequent testing confirmed that pituitary function was normal.

figure 3This patient had a glycoprotein-secreting pituitary tumor, also known as a nonfunctioning pituitary tumor. The tumor usually occurs in older men who present with erectile dysfunction and headaches.

Once considered uncommon, glycoprotein-secreting pituitary tumors are now recognized as the second most common pituitary tumor. Prolactinomas are the most common, accounting for about 40% of cases. Growth hormone-secreting tumors, which cause acromegaly, account for about 10% of cases; ACTH-secreting tumors, which cause Cushing’s syndrome, cause 10% or fewer of pituitary tumors.

Pituitary tumors occur in about one in 10,000 persons. Until recently, many physicians did not look for these tumors, which escaped notice until they grew very large. Now that evaluation for hypogonadism in men with erectile dysfunction is being done more frequently, the tumors are being detected at an earlier stage.

The urologic literature used to recommend against performing a hormonal evaluation in men with erectile dysfunction, because a hormonal cause was found in less than 10% of cases. However, that figure reflected the experience in urologic practices, which assess large numbers of younger men with stress-induced erectile dysfunction. In a retrospective study of 100 men with erectile dysfunction seen at my endocrine impotence clinic, which serves an older group of patients with multiple systemic diseases, 48% of cases had a hormonal component. It was not necessarily the only cause–they also may have had vascular or neurogenic problems–but it was important enough not to miss, because treatment will not succeed if only part of the problem is addressed. Evaluation for hormonal deficiency is also important because there are many other risks associated with longstanding hypogonadism, such as osteoporosis and premature exacerbation of cardiovascular disease (probably due to estrogen deficiency, which occurs with loss of androgens).

It was previously thought that if a patient had a defect in pituitary hormone production before surgery, it meant that the pituitary had been irrevocably damaged, and that the patient would require life-long replacement therapy after the surgery. We now know that when the operation is performed by a skilled neurosurgeon who is able to remove the tumor while preserving the pituitary, normal pituitary function can return. About six weeks after surgery, hormone replacement therapy is stopped and patients are retested. If the surgery was successful, the prognosis is very good. Periodic follow-up with MRI scans is indicated to detect recurrences, but they are rare.

Should hypogonadotropic hypogonadism persist after tumor removal, the patient will need androgen replacement for androgenization or, to restore fertility, treatment with either human chorionic gonadotropin or pulsatile gonadotropin- releasing hormone (GnRH). At present, I use testosterone patches for androgen replacement. The patches are more expensive than intramuscular testosterone injections but allow closer mimicking of the normal diurnal variation in testosterone levels. The results are noticeable within a week of starting treatment of male stamina enhancement.

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Doesn’t the sight of Brad Pitt, Tom Cruise, Antonio Banderas give you goose bumps? Your heart skips a beat and you wonder what is it about these Hollywood hunks, apart from their perfect face and body that makes heads turn. Well, it is the charm and the charisma that oozes from every pore of their body, that look in their eye or that killer smile which floors millions of women. You may not actually be a Tom cruise or a Meg Ryan, but you could be as devastating and have the same fan following. Only if you perfect the art of flirting.

What exactly is flirting? Flirting is expressing your feeling of attraction via your words and deeds in such a way that the other person is irresistibly drawn to you. Flirting is not practical or direct but cleverly and subtly done through the use of body language, intonations and suggestions. Do you know that all of us flirt but some people are better than others? Here is how men and women flirt. Try incorporating some of these basic moves into your behavior and see your fan following grow:
Five things men do when they flirt:

* Arch his back and puff his chest, usually by leaning back in a chair and putting his arms behind his head. This will be accompanied by a sweet smile.
* Stretch the chest muscles, which is interpreted as a sign of their ability to protect.
* Swaying the pelvis just like Elvis, chances are that he has the hots for you.
* Tugging his tie is a common giveaway. It indicates nervousness.
* Clasping the back of his neck. Other gestures may include pointing his chin up in the air or placing palms on a table or their knees. While the former means showing off his rugged features, the latter is a reassurance of harmlessness.

Five things women do when they flirt:

* Smile: When a woman smiles at her admirer it signals availability and interest.
* Arching eyebrows so as to gaze wide-eyed, or quickly lowering their lids, tucking their chin and averting the gaze.
* Giggle: Normally done by placing the hand over or near the mouth, a sign of youth and submissiveness. This is often accompanied by that slight shrug of the shoulders sometimes interpreted as a sign of helplessness.
* Tossing their mane is something that most men just cannot resist. Or walking with a gentle sway of the hips calling attention to the pelvis and advertising curves.
* Rolling the tongue over the lips signals sexual maturity and interest.

Some people are born flirts, while others learn along the way. If you master these techniques you too could become an ace charmer. All you need is a bit of creativity, originality and subtle body language and you will be a fabulous flirt all your life.

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