Associated morbidity may include various other male sexual dysfunctions, such as premature (early) ejaculation and male hypoactive sexual desire disorder. The NHSLS found that 28.5% of men aged 18-59 years reported premature ejaculation, and 15.8% lacked sexual interest during the past year. An additional 17% reported anxiety about sexual performance, and 8.1% had a lack of pleasure in sex. 
Besides PDE5 inhibitors and among second-line therapies are VCDs which are clear plastic chambers placed over the penis, tightened against the lower abdomen with a mechanism to create a vacuum inside the chamber. This directs blood into the penis. If an adequate erection occurs inside the chamber, the patient slips a small constriction band off the end of the VCD and onto the base of the penis. An erection beyond 30 min is not recommended. These devices can be a bit cumbersome, but are very safe.40
Occasional successful sexual function and early morning erections do not preclude the possibility of endocrine dysfunction. Since abnormally low levels of testosterone frequently are the primary cause of impotence, it is recommended that determination of the blood level of testosterone be an integral part of the total evaluation of the impotent patient.
Another study compared the response of surgically and medically castrated rabbits to vardenafil with that of control rabbits.  Castrated rabbits did not respond to vardenafil, whereas noncastrated rabbits did respond appropriately. This result suggests that a minimum amount of testosterone is necessary for PDE5 inhibitors to produce an erection.
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Trauma to the pelvic blood vessels or nerves can also lead result in ED. Bicycle riding for long periods has been implicated as an etiologic factor; direct compression of the perineum by the bicycle seat may cause vascular and nerve injury.  On the other hand, bicycling for less than 3 hours per week may be somewhat protective against ED.  Some of the newer bicycle seats have been designed to diminish pressure on the perineum. [37, 38]
This is one of many types of constricting devices placed at the base of the penis to diminish venous outflow and improve the quality and duration of the erection. This is particularly useful in men who have a venous leak and are only able to obtain partial erections that they are unable to maintain. These constricting devices may be used in conjunction with oral agents, injection therapy, and vacuum devices.
Appallingly little is known about the prevalence of erectile dysfunction in the United States and how this prevalence varies according to individual characteristics (age, race, ethnicity, socioeconomic status, and concomitant diseases and conditions). Data on erectile dysfunction available from the 1940's applied to the present U.S. male population produce an estimate of erectile dysfunction prevalence of 7 million.
This may be the oldest excuse in the book as a reason not to have safe sex, but research has confirmed that condoms may interfere with some men’s ability to have and hold an erection. For example, a 2006 study found that, over a three-month period, about 37 percent of men lost at least one erection when putting on a condom, or during sex with a condom, SexualHealth.com reported.
For some patients with an established diagnosis of testicular failure (hypogonadism), androgen replacement therapy may sometimes be effective in improving erectile function. A trial of androgen replacement may be worthwhile in men with low serum testosterone levels if there are no other contraindications. In contrast, for men who have normal testosterone levels, androgen therapy is inappropriate and may carry significant health risks, especially in the situation of unrecognized prostate cancer. If androgen therapy is indicated, it should be given in the form of intramuscular injections of testosterone enanthate or cypionate. Oral androgens, as currently available, are not indicated. For men with hyperprolactinemia, bromocriptine therapy often is effective in normalizing the prolactin level and improving sexual function. A wide variety of other substances taken either orally or topically have been suggested to be effective in treating erectile dysfunction. Most of these have not been subjected to rigorous clinical studies and are not approved for this use by the Food and Drug Administration (FDA). Their use should therefore be discouraged until further evidence in support of their efficacy and indicative of their safety is available.
The U.S. FDA (Food and Drug Administration) has a list of 29 OTC products that claim to treat erectile dysfunction. Patients should avoid these because many contain harmful ingredients. Other natural or herbal remedies such as DHEA, L-arginine, ginseng, and yohimbe are supplements that have been used but have not been proven safe and effective according to some researchers. Before using such compounds, individuals should consult their doctor. According to some experts, acupuncture does not effectively treat erectile dysfunction. Other home remedies for reducing ED symptoms include diet changes such as eating blueberries and citrus fruits and drinking red wine.
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
Another potential new treatment consists of penile low-intensity shock wave lithotripsy. This consists of 1500 shocks twice a week for 3–6 weeks. The purpose is to stimulate neovascularisation to the corporal bodies with improvement in penile blood flow and endothelial function. The use of low-intensity shock wave lithotripsy may convert PDE5 inhibitor non-responders to responders.47
Unfortunately, some patients may have an overly simplified understanding of the role of PDE5 inhibitors in ED management. Such patients may not expect or be willing to undergo a long evaluation and testing process to obtain a better understanding of their sexual problem, and they may be less likely to involve their partner in discussing their sexual relationship with the physician. They may expect to obtain medications through a phone call to their doctor or even over the Internet, with minimal or no physician contact at all.
The rumors are true. Having too much to drink can interfere with a man’s ability to have an erection. According to Everyday Health, alcohol is a depressant. This means that, along with dampening your ability to think, speak, and move efficiently, it can also dampen mood, decrease sexual desire, and make it difficult for a man to achieve erection or reach an orgasm. This is because alcohol decreases blood flow to the penis. That not only may reduce a man’s ability to have an erection, but even if he is lucky enough to get it hard, alcohol can reduce the intensity of his orgasm.
Alprostadil should not be used in men at higher risk for priapism (erection lasting longer than six hours) including men with sickle cell anemia, thrombocytopenia (low platelet count), polycythemia (increased red blood cell count), multiple myeloma (a cancer of the white blood cells), and is contraindicated in men prone to venous thrombosis (blood clots in the veins) or hyperviscosity syndrome who are at increased risk for priapism.
Additionally, the physiologic processes involving erections begin at the genetic level. Certain genes become activated at critical times to produce proteins vital to sustaining this pathway. Some researchers have focused on identifying particular genes that place men at risk for ED. At present, these studies are limited to animal models, and little success has been reported to date.  Nevertheless, this research has given rise to many new treatment targets and a better understanding of the entire process.
Quitting smoking, exercising regularly, losing excess weight, curtailing excessive alcohol consumption, controlling hypertension, and optimizing blood glucose levels in patients with diabetes are not only important for maintaining good health but also may improve or even prevent progression of erectile dysfunction. It is unclear if such lifestyle changes can reverse erectile dysfunction. However, lifestyle improvements may prevent progression of the erectile dysfunction. Some studies suggest that men who have made lifestyle improvements experience increased rates of success with oral medications.
On the horizon is gene therapy that would deliver genes that produce products or proteins that may not be functioning properly in the penile tissue of men with ED. Replacement of these proteins may result in improvement in erectile function. Experimental animal models have demonstrated improvement in erectile function with gene therapy. Human studies may also demonstrate success with this therapy. Gene therapy may take a long time for regulatory approval and public acceptance.
What’s important to take away from this is that, because erections can occur throughout the day for no reason, erectile dysfunction can be difficult to diagnose. Some men achieve erections for no reason, yet when provided with stimuli, they aren’t able to. Some men, on the other hand, only get aroused when directly stimulated. This means that healthcare professionals need to take into account many variables prior to diagnosing and treating erectile dysfunction.