"Medications that create blood flow to the penis can't help when an erection is blocked by the fear or anxiety of the fight-or-flight response,” says Feloney. “This type of erectile dysfunction probably has a lot to do with evolution — men didn't need an erection when a dinosaur was chasing them." The best way to treat erectile dysfunction caused by performance anxiety, depression, a poor relationship, or stress may be with a combination of ED drug treatment and sex therapy, individual therapy, or couples therapy from sexual health professionals.
ED is often the result of atherosclerosis, and as a result, men with ED frequently have cardiovascular disease. Sexual activity is associated with increased physical exertion, which in some men may increase the risk of having a heart attack (myocardial infarction or MI). The major risk factors associated with cardiovascular disease are age, hypertension, diabetes mellitus, obesity, smoking, abnormal lipid/cholesterol levels in the blood, and lack of exercise. Individuals with three or more of these risk factors are at increased risk for a heart attack during sexual activity. The Princeton Consensus Panel developed guidelines for treating ED in men with cardiovascular disease. Thus, if you have ED and cardiovascular disease (for example, angina or prior heart attack), you should discuss whether or not treatment of ED and sexual activity are appropriate for you.
Sexual dysfunction and ED become more common as men age. The percentage of complete ED increases from 5% to 15% as age increases from 40 to 70 years. But this does not mean growing older is the end of your sex life. ED can be treated at any age. Also, ED may be more common in Hispanic men and in those with a history of diabetes, obesity, smoking, and hypertension. Research shows that African-American men sought medical care for ED twice the rate of other racial groups.
Erectile dysfunction (ED) related to compromise of the nervous system is an increasingly common occurrence. This may be due to the multifactorial nature of ED, the myriad of disorders affecting the neurotransmission of erectogenic signals, and improved awareness and diagnosis of ED. Nevertheless, neurogenic ED remains poorly understood and characterized. Disease related factors such as depression, decreased physical and mental function, the burden of chronic illness, and loss of independence may preclude sexual intimacy and lead to ED as well. The amount of data regarding treatment options in subpopulations of differing neurologic disorders remains scarce except for men with spinal cord injury. The treatment options including phosphodiesterase inhibitors, intracavernosal or intraurethral vasoactive agents, vacuum erection devices (VED) and penile prosthetic implantation remain constant. This review discusses the options in specific neurologic conditions, and briefly provides insight into new and future developments that may reshape the management of neurogenic ED.
These oral medications reversibly inhibit penile-specific PDE5 and enhance the nitric oxide–cGMP pathways of cavernous smooth muscle relaxation; that is, all prevent the breakdown of cGMP by PDE5. It is important to emphasize to patients that these drugs augment the body’s natural erectile mechanisms, therefore the neural and psychoemotional stimuli typically needed for arousal still need to be activated for the drugs to be efficacious.
Aging: There are two reasons why older men are more likely to experience erectile dysfunction than younger men. First, older men are more likely to develop diseases (such as heart attacks, angina, cardiovascular disease, strokes, diabetes mellitus, and high blood pressure) that are associated with erectile dysfunction. Second, the aging process alone can cause erectile dysfunction in some men by causing changes in the muscle and tissue within the penis.
Clinical experience in switching medications to improve ED has been disappointing in that improvement does not often occur. Nonetheless, it is important to try to discontinue possible offending medications before proceeding to more invasive ED treatment options. Oral ED medications have changed the way clinicians discontinue medications in patients with ED and has improved the approach. For example, a patient may develop ED on a thiazide diuretic. The diuretic may be withdrawn, but a trial of oral ED therapy can be initiated during the observation period while the patient is waiting to see if any spontaneous improvement in ED occurs after drug withdrawal. Alternatively, if diuretic therapy is effective, well tolerated, and controlling blood pressure, oral ED therapy can be used on an ongoing basis to treat the side effect of ED.
The vacuum constriction device consists of a vacuum cylinder, various sizes of tension rings, and a vacuum pump, either hand-operated or electric. The penis is placed in a cylinder to which a tension ring is attached. Air is evacuated from the cylinder by means of the pump, creating a vacuum, which produces the erection. The cylinder is removed, leaving the tension ring at the base of the penis to maintain the erection.
Yes, the vacuum device is effective. In fact, with use of the vacuum device, 88% of men will have an erection that is satisfactory for completion of sexual activity. The vacuum device may be the only therapy that is effective after the removal of a penile prosthesis. Patients also use vacuum devices as part of penile rehabilitation after radical prostatectomy to help preserve the tissue of the penis and prevent scarring within the penis and loss of penile length. Its use, however, is limited by the mechanical nature of it and the time taken to pump the device and apply the band. Sex partners may complain of the penis being cool to touch.
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.
Medications: Many common medicines produce erectile dysfunction as a side effect. Medicines that can cause erectile dysfunction include many used to treat high blood pressure, antihistamines, antidepressants, tranquilizers, and appetite suppressants. Examples of common medicines that can cause erectile dysfunction include propranolol (Inderal) or other beta-blockers, hydrochlorothiazide, digoxin (Lanoxin), amitriptyline (Elavil), famotidine (Pepcid), cimetidine (Tagamet), metoclopramide (Reglan), naproxen, indomethacin (Indocin), lithium (Eskalith, Lithobid), verapamil (Calan, Verelan, Isoptin), phenytoin (Dilantin), gemfibrozil (Lopid), amphetamine/dextroamphetamine (Adderall), and phentermine. Prostate cancer medications that lower testosterone levels such as leuprolide (Lupron) may affect erectile function. Some chemotherapies such as cyclophosphamide (Cytoxan) may affect erectile function.
However, a review of a United Kingdom medical record database found no evidence that the use of 5-alpha reductase inhibitors independently increase the risk for ED. In 71,849 men with benign prostatic hyperplasia (BPH), the risk of ED was not increased with the use of finasteride or dutasteride only (odds ratio [OR] 0.94), or a 5-alpha reductase inhibitor plus an alpha blocker (OR 0.92) compared with an alpha blocker only. In addition, the risk of ED was not increase in 12 346 men prescribed finasteride 1 mg for alopecia, compared with unexposed men with alopecia (OR 0.95). The risk of ED did increase with longer duration of BPH, regardless of drug exposure. 
Alprostadil (also known as prostaglandin E1 [PGE1]) is the prominent known smooth-muscle dilator of the corpus cavernosum. Its mechanism of action is believed to be the promotion of intracellular accumulation of cyclic adenosine monophosphate, thereby causing decreased intracellular accumulation of calcium and resulting smooth muscle relaxation. Alprostadil can be delivered to the erectile tissue either via an intraurethral suppository that is massaged and then absorbed across the corpus spongiosum of the urethra to the corpora cavernosa, or directly injected into the corpora cavernosa. When administered urethrally, doses are substantially higher than when directly injected (typical dosing is 500 mcg to 1 mg intraurethral compared with 2.5 mcg to 20 mcg intracavernosal).
With an inflatable implant, fluid-filled cylinders are placed lengthwise in the penis. Tubing joins these cylinders to a pump placed inside the scrotum (between the testicles). When the pump is engaged, pressure in the cylinders inflate the penis and makes it stiff. Inflatable implants make a normal looking erection and are natural feeling for your partner. Your surgeon may suggest a lubricant for your partner. With the implant, men can control firmness and, sometimes, the size of the erection. Implants allows a couple to be spontaneously intimate. There is generally no change to a man's feeling or orgasm.