The FDA does not recommend alternative therapies to treat sexual dysfunction.[24] Many products are advertised as "herbal viagra" or "natural" sexual enhancement products, but no clinical trials or scientific studies support the effectiveness of these products for the treatment of erectile dysfunction, and synthetic chemical compounds similar to sildenafil have been found as adulterants in many of these products.[25][26][27][28][29] The United States Food and Drug Administration has warned consumers that any sexual enhancement product that claims to work as well as prescription products is likely to contain such a contaminant.[30]
A meta-analysis of 36 744 men with ED in 12 prospective cohort studies found that the presence of ED significantly increased the risk of CVD, CAD, stroke and all-cause mortality, and the presence of ED was an independent risk factor for CVD. Ponholzer et al found that men with moderate to severe ED had a 65% increased relative risk for developing symptomatic CAD compared with men who did not have ED.26
Penile prostheses are very effective, and most patients who have a prosthesis placed are satisfied with the prosthesis. However, placement of a prosthesis causes scarring of the tissue within the corpora cavernosa, and if the prosthesis requires removal, other forms of therapy, except for the vacuum device, are often not effective. Thus, most physicians reserve placement of a prosthesis for men who have tried and failed or have contraindications to other therapies.
Normal erectile function depends on the release of NO and endothelial-dependent vasodilation of the penile arteries. The ‘artery size’ hypothesis, first described by Dr Montorsi, offers an explanation why men are more likely to develop ED before a myocardial infacrtion. It is believed that atherosclerosis affects all vascular beds equally but smaller arteries are more likely to become occluded than larger arteries.31 32 The penile arteries are 1–2 mm while the coronary arteries are 3–4 mm. Thus, the same degree of endothelial dysfunction and atherosclerosis is more likely to occlude blood flow in the penile arteries compared with the coronary arteries. The penile arteries therefore serve as a sensitive indicator for subsequent CVD. This theory is supported by the fact that ED occurs approximately 3 years prior to cardiac symptoms in virtually all patients with chronic coronary syndrome whereas patients with acute coronary syndrome have a much lower prevalence of sexual dysfunction.32

Studies to further define vasculogenic disorders include pharmacologic duplex grey scale/color ultrasonography, pharmacologic dynamic infusion cavernosometry/ cavernosography, and pharmacologic pelvic/penile angiography. Cavernosometry, duplex ultrasonography, and angiography performed either alone or in conjunction with intracavernous pharmacologic injection of vasodilator agents rely on complete arterial and cavernosal smooth muscle relaxation to evaluate arterial and veno-occlusive function. The clinical effectiveness of these invasive studies is severely limited by several factors, including the lack of normative data, operator dependence, variable interpretation of results, and poor predictability of therapeutic outcomes of arterial and venous surgery. At the present time these studies might best be done in referral centers with specific expertise and interest in investigation of the vascular aspects of erectile dysfunction. Further clinical research is necessary to standardize methodology and interpretation, to obtain control data on normals (as stratified according to age), and to define what constitutes normality in order to assess the value of these tests in their diagnostic accuracy and in their ability to predict treatment outcome in men with erectile dysfunction.

It is necessary to identify the causes of worry and try to remove these. They could include concern about personal relationships, work, family problems, health or even sexual “performance” with a new or old partner. It is often said that the brain is the biggest sex organ of them all – if it is too busy with other things, it will not be involved in arousal and the erection that follows.
Erections are neurovascular events, meaning that nerves and blood vessels (arteries and veins) are involved in the process of an erection and all must work properly to develop a hard erection that lasts long enough. Erection begins with sexual stimulation. Sexual stimulation can be tactile (for example, by a partner touching the penis or by masturbation) or mental (for example, by having sexual fantasies, viewing porn). Sexual stimulation or sexual arousal causes the nerves going to the penis to release a chemical, nitric oxide. Nitric oxide increases the production of another chemical, cyclic GMP (cGMP), in the muscle of the corpora cavernosa. The cGMP causes the muscles of the corpora cavernosa to relax, and this allows more blood to flow into the penis. The incoming blood fills the corpora cavernosa, making the penis expand.

*All medications have both common (generic) and brand names. The brand name is what a specific manufacturer calls the product (e.g., Tylenol®). The common name is the medical name for the medication (e.g., acetaminophen). A medication may have many brand names, but only one common name. This article lists medications by their common names. For information on a given medication, check our Drug Information database. For more information on brand names, speak with your doctor or pharmacist.
Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.
Little is known about the natural history of erectile dysfunction. This includes information on the age of onset, incidence rates stratified by age, progression of the condition, and frequency of spontaneous recovery. There also are very limited data on associated morbidity and functional impairment. To date, the data are predominantly available for whites, with other racial and ethnic populations represented only in smaller numbers that do not permit analysis of these issues as a function of race or ethnicity.
This is similar to magnetic resonance imaging. Magnetic resonance angiography uses magnetic fields and radio waves to provide detailed images of the blood vessels. Doctors may inject a "contrast agent" into the patient's bloodstream that causes vascular tissues to stand out against other tissues. The contrast agent provides for enhanced information regarding blood supply and vascular anomalies.
Since no two men are alike, the best ED treatment plan will depend on what’s causing your problem. That’s why you need to put aside your embarrassment and make an appointment to visit with see a qualified doctor who specializes in helping guys get back to enjoying their time with their spouses or partners to the fullest. You’ll be relieved to talk to someone who understands and has solutions.
To start with, ED is NOT in your head. You can’t simply will yourself to get an erection, no matter how much you try. Studies show over 80% of ED cases are caused by a treatable physical disorder. Diseases such as diabetes, high blood pressure, and high cholesterol are common causes. Even a perfectly healthy man can develop ED after a brain or spinal cord injury. ED can be a side effect of certain medications, too.  Read more on our Causes of ED page.
Talk with your doctor before trying supplements for ED. They can contain 10 or more ingredients and may complicate other health conditions. Asian ginseng and ginkgo biloba (seen here) are popular, but there isn't a lot of good research on their effectiveness. Some men find that taking a DHEA supplement improves their ability to have an erection. Unfortunately, the long-term safety of DHEA supplements is unknown. Most doctors do not recommend using it.
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