Erectile dysfunction (ED) is a serious, life-altering problem for millions of men. A man’s inability to achieve or maintain an erection is inevitably linked to complex feelings of inadequacy, frustration, and shaken confidence, which may spill over into other areas of his life. The psychological and quality-of-life consequences of ED must not be underestimated.
Since the introduction of Viagra® (sildenafil citrate) in 1998, several other drugs for the treatment of ED have been introduced; it has become clear that ED is far more prevalent than may have been suspected previously. A study conducted in the Boston area from 1987 to 1989 found that 52 percent of men between the ages of 40 and 70 suffered some degree of ED (Feldman HA et al 1994). By extrapolation, about 30 million men are affected by ED in the United States (McKay D 2004). And given men’s ever increasing lifespan, it has been further estimated that the incidence of ED worldwide will more than double in the next quarter century (Goldstein I 2000).
Clearly, Viagra® and drugs like it are blockbusters for their manufacturers. They have improved the quality of life for countless millions of men and their partners who might otherwise have faced either years of continued impotence or unpleasant and possibly unsatisfactory alternatives, such as penile implants or penile injections. But these medications have their drawbacks. Despite their resounding success in the marketplace, ED drugs produce a number of side effects (some serious, such as the small risk of blindness) (Akash R et al 2005), and not all men can take them. For about 30 percent of patients, ED drugs don’t work to patients’ satisfaction (Sussman DO 2004). This high failure rate has prompted researchers to search for alternatives.
Over the centuries, countless products have been touted as enhancing male vigor and increasing libido. While the effectiveness of many of these substances cannot be adequately proved or disproved, several candidates have demonstrated some degree of efficacy in controlled human trials.
It may also be important for men to test their blood levels of free testosterone and estradiol (an estrogen). As men age, they often suffer from a deficiency of free testosterone while producing too much estrogen. Sexual desire and performance are strongly affected by these hormones. The good news is that there are safe ways of increasing free testosterone and reducing excess estrogen, which can lead to a significant improvement in a man’s sexual satisfaction.
Anatomy of an Erection
The penis is largely under the control of the central nervous system. The features that allow erection to occur consist of spongy columns of tissue known as the corpus cavernosum and corpus spongiosum. When these specialized tissues engorge with blood, erection is achieved. This process, however, is quite complicated, involving complex interactions among psychological and physical stimuli and chemical signals, as well as a shifting balance between inhibitory and excitatory forces.
During sexual stimulation, the brain sends signals that result in the release of nitric oxide by parasympathetic neurons in the penis. Penile endothelial cells are also stimulated to release nitric oxide. As nitric oxide diffuses into the smooth-muscle cells lining the arteries of the corpus cavernosum and corpus spongiosum, it stimulates the activation of an enzyme called guanylate cyclase. This enzyme produces cyclic guanosine monophosphate (cGMP), which prompts the smooth muscles of penile arteries to relax, allowing more blood to flow into the spongy tissues of the penis. Simultaneously, blood return via penile veins is restricted, trapping blood in the organ, resulting in engorgement and erection.
Eventually, cGMP is broken down by phosphodiesterase type 5 enzymes (PDE5). When this occurs, the erection subsides; blood flow returns to normal, and the penis resumes its normal flaccid state. The chain of events leading to erection presents several opportunities for intervention in the treatment of ED. Increasing the availability of nitric oxide is one, while decreasing the activity of PDE5 is another.
Viagra®, Cialis®, and Levitra® (vardenafil), for instance, are selective inhibitors of PDE5. By inhibiting the degradation of cGMP, which is the direct intracellular mediator of the nitric oxide pathway, these drugs promote better erections—but not without side effects and risks. For example, all the drugs in this class are contraindicated for men taking nitric oxide–donor drugs, such as organic nitrates for cardiovascular conditions. Mixing these drugs may result in dangerously low blood pressure. Viagra® may temporarily affect color vision and in rare cases may cause blindness (Akash R et al 2005). And any of these drugs may induce a sustained erection that does not subside after more than four hours—a potentially damaging condition known as priapism. Less-severe side effects commonly associated with this class of drugs include headaches, nasal congestion, and flushing (Gresser U et al 2002).
Testosterone Therapy for ED
Testosterone is well known as the primary “male hormone.” In aging men with ED, returning testosterone to youthful levels appears to make perfect sense, given testosterone’s association with vigor, libido, and masculinity. However, the actual situation is more complicated.
While it is fairly well established that testosterone plays a role in libido, or sexual desire, its precise contribution to erectile function remains unclear (Martinez-Jabaloyas JM et al 2006; Mikhail N 2006; Traish AM et al 2006). ED occurs in men with normal or moderately low levels of testosterone, so it cannot be concluded that testosterone is the primary modulator of erectile function.
But among men diagnosed with hypogonadism—a condition characterized by abnormally low testosterone—erections do, in fact, improve after testosterone supplementation. For these men with ED, testosterone therapy is recommended to maintain secondary sex characteristics and restore erectile function (Bhasin S et al 2006). Recent evidence suggests that “a significant proportion of men [older than] 60 years of age have biochemical hypogonadism” (Caretta N et al 2005).
Testosterone replacement therapy has also been recommended as a second-line approach to treatment of ED when prescription medications alone have failed and when prostate cancer has been ruled out (Mikhail N 2006; Rosenthal BD et al 2006; Yassin AA 2006; Morales A et al 2004). As an added bonus, new data suggest that testosterone tends to reduce inflammation, a chronic condition associated with aging and degenerative processes (Maggio M 2005).
However, it is important to note that because of testosterone’s role in encouraging the growth of certain types of prostate cancer, supplementation with this hormone is not without risk. Among patients with advanced prostate cancer, current therapies are actually designed to suppress testosterone rather than boost it (Altwein J et al 2006; Berges R et al 2006). But testosterone therapy appears to be safe and beneficial for men who are free of prostate cancer.
The bottom line is this: aging men who don’t respond to other ED treatments may benefit from testosterone-boosting therapy. In these patients, restoring testosterone to youthful levels may actually be the key to restoring normal erectile function (Gooren LJ et al 2006).
Testosterone replacement should be explored with caution. It is crucial to rule out prostate cancer before considering testosterone therapy. Once prostate health is established, a physician may prescribe testosterone replacement therapy. But an alternative approach exists that doesn’t require a drug prescription. It is possible to increase circulating testosterone levels by preventing the conversion of testosterone to estrogen in the body.
Certain drugs and supplements can inhibit the activity of aromatase, an enzyme that facilitates the transformation of testosterone into estrogen (Kijima I et al 2006; T’Sjoen GG et al 2005; Eng ET et al 2002, 2003). One such aromatase inhibitor is grape seed extract. It has been shown to be useful in the treatment of estrogen-dependent breast cancer, due to its ability to prevent the conversion of androgens (male hormones) to estrogens. Resveratrol, also derived from grapes, has been found to inhibit aromatase (Wang Y et al 2006). Chrysin is another plant-derived aromatase inhibitor. Although the bioavailability of chrysin by itself is problematic, the addition of piperine greatly increases the absorbability of this testosterone-boosting phytochemical (Khajuria A et al 2002). Finally, zinc may be of benefit in helping to boost testosterone through inhibition of aromatase (Kaya O et al 2006; He F et al 2005).
The hormone progesterone also acts as a 5-alpha reductase inhibitor (Tilakaratne A et al 2000; Schmidt M et al 1998).
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