Patients who use this therapy should be trained under the guidance of a urologist, and sterile technique must be used. The drugs must be injected into the shaft of the penis and into one of the penile erectile bodies (corpus cavernosum) 10–15 min before intercourse. Most patients do not complain of pain upon injection. Sexual stimulation is not required, and resulting erections may last for hours. Side effects include penile pain and priapism. The cost is about $12–20 per injection.
Diabetes, high blood pressure (hypertension), elevations in blood lipids or cholesterol are considered blood vessel problems and have all been associated with Erectile Dysfunction. The blood vessel abnormalities caused by these diseases affect vessels throughout the body and often produce other symptoms of vascular diseases. Diabetics and patients with hypertension frequently have heart disease. These conditions typically interfere with the ability of the penile vessels to work properly and ultimately cause ED.
L-arginine, an amino acid that is naturally present in the body and helps make nitric oxide, supports a successful erection. Nitric oxide is responsible for making the blood vessels relax, which helps sustain an erection for men. A 1999 study, observed the effects of six weeks of high-dose (5 grams/day) orally administered nitric oxide (NO) donor L-arginine on men with organic ED. Thirty-one percent of those who took 5 grams/day of L-arginine experienced significant improvements in sexual function. Burns told Medical Daily, “l-arginine and deer antler velvet” have been the most popular go-to natural treatments for men.
If you take a diuretic, you should stay on it until high blood pressure is under control. If erection problems persist, or blood pressure goes back up, then your doctor might switch to a drug that's less likely to cause erectile dysfunction. Or, a combination of medications might work better to control high blood pressure and lower the risk of erectile dysfunction.
Crossref | PubMed | Scopus (539) | Google ScholarSee all References The MMAS 9-year follow-up study has shown that a body mass index of 28 kg/m2 or higher was an independent predictor for ED, with an adjusted odds ratio of 1.96.5x5Feldman, HA, Johannes, CB, Derby, CA et al. Erectile dysfunction and coronary risk factors: prospective results from the Massachusetts Male Aging Study. Prev Med. 2000; 30: 328–338
DHEA is a hormone made by the human body. It’s a building block for testosterone. According to a study published in Urology, this supplement may be able to help men whose ED is related to having low testosterone. However, there’s no definitive evidence of this benefit. It’s clear that DHEA can cause various side effects, including liver damage and acne. Long-term use of DHEA can also cause hormonal imbalances.
Few simple laboratory tests can help identify obvious causes of organic ED. Initial labs should include HbA1c, free testosterone, thyroid function tests, and prolactin levels. However, patients who do not respond to pharmacological therapy or who may be candidates for surgical treatment may require more in-depth testing, including nocturnal penile tumescence testing, duplex Doppler imaging, somatosensory evoked potentials, or pudendal artery angiography.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (272) | Google ScholarSee all References Between 1987 and 1989, the Massachusetts Male Aging Study (MMAS), a community-based random sample observational study of 1709 men, used self-administered sexual activity questionnaires to gather information about noninstitutionalized men aged 40 to 70 years in cities near Boston.4x4Feldman, HA, Goldstein, I, Hatzichristou, DG, Krane, RJ, and McKinlay, JB. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol. 1994; 151: 54–61
4. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Erectile dysfunction (updated Nov 2015). https://www.niddk.nih.gov/health-information/health-topics/urologic-disease/erectile-dysfunction/Pages/facts.aspx (accessed Nov 2016). myDr myDr provides comprehensive Australian health and medical information, images and tools covering symptoms, diseases, tests, medicines and treatments, and nutrition and fitness.Related ArticlesImpotence causesFind out the physical and psychological causes of impotence, also called erectile dysfunction or ED.Erectile dysfunction: visiting your doctorFind out what questions a doctor may ask when discussing erectile dysfunction (ED, or impotence8 Surprising causes of erectile dysfunctionOccasional erectile dysfunction is not uncommon, but if it's persistent, erectile dysfunction caAdvertisement
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References The risk after sexual activity in these patients is unknown, although vasodilators should be avoided because they may increase the intraventricular gradient.51x51DeBusk, R, Drory, Y, Goldstein, I et al. Management of sexual dysfunction in patients with cardiovascular disease: recommendations of the Princeton Consensus Panel. Am J Cardiol. 2000; 86: 62F–68F
Ginseng, specifically “red ginseng,” is known as the “herbal Viagra” that helps puts to rest men’s bedroom woes. Red ginseng is when the root has been steamed and then dried. The ginseng root is the part of the plant that is mostly used as a natural remedy when in its supplement form. However, the plant must be grown for a minimum of five years before it can be used. In a 2008 review, seven studies on red ginseng and ED, ranging in dosages from 600 to 1,000 milligrams three times a day, were found to provide evidence for the effectiveness of the herb in ED treatment.

A penile prosthesis is another treatment option for men with erectile dysfunction. These devices are either malleable (bendable) or inflatable. The simplest type of prosthesis consists of a pair of malleable rods surgically implanted within the erection chambers of the penis. With this type of implant the penis is always semi-rigid and merely needs to be lifted or adjusted into the erect position to initiate sex. Today, many men choose a hydraulic, inflatable prosthesis, which allows a man to have an erection whenever he chooses and is much easier to conceal. It is also more natural.
When these drugs don't work, there are other options. Medications that dilate blood vessels, such as alprostadil, can be injected or deposited in the penis; they work in more than 80 percent of men with diabetes. Beyond that, penile implants can be an effective surgical solution. Implants are either malleable rods, which can be manually adjusted to the desired position, or inflatable cylinders that fill with fluid when a pump under the skin of the scrotum is pressed.

The natural history of ED in people with diabetes is normally gradual and does not occur overnight. Both vascular and neurological mechanisms are most commonly involved in people with diabetes. Atherosclerosis in the penile and pudendal arteries limits the blood flow into the corpus cavernosum. Because of the loss of compliance in the cavernous trabeculae, the venous flow is also lost. This loss of flow results in the inability of the corpora cavernosae to expand and compress the outflow vessels.
The use of shock wave therapy has revolutionized the treatment of many aspects of medicine. High intensity extracorporeal shockwave therapy has been used for the treatment of nephro-urolithiasis while medium intensity shockwave therapy is used by orthopaedic surgeons to treat joint pain as well as tendinitis. Low intensity shockwaves therapy was first noted to improve ischaemia-induced myocardial dysfunction in animal studies when low intensity shockwaves were applied to porcine myocardium (13). Shockwaves induces a localized stress on cell membranes in the same way that shear stress affects endothelial cell membranes (14) and this triggers the release of angiogenic factors, such as increased NO production through increased activity of endothelial NO synthase (eNOS) and neuronal NO synthase (nNOS), platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) (15). These shockwaves also cause membrane hyperpolarization (16), activation of the Ras signaling pathway, non-enzymatic synthesis of NO and induction of stress fibers and intercellular gaps (17).
Crossref | PubMed | Scopus (171) | Google ScholarSee all References Incidence increased notably with age in this patient cohort: only 1.1% of diabetic men aged 21 to 30 years had ED compared with 47.1% of all diabetic patients older than 43 years. Diabetic patients often have other cardiovascular risk factors that may play a role in the development of ED. However, in an analysis of the PBI in 441 patients with ED and various cardiovascular risk factors (diabetes mellitus, hypertension, hyperlipidemia, tobacco use), diabetes was the only risk factor that was significantly and independently associated with a decrease in the PBI.7x7Virag, R, Bouilly, P, and Frydman, D. Is impotence an arterial disorder? a study of arterial risk factors in 440 impotent men. Lancet. 1985; 1: 181–184
The drugs come in several strengths. Most men should start with a low to moderate dose. The dose can be adjusted depending on the results. Men with potential problems should always start with the lowest dose. Every man should avoid consuming alcohol before taking these drugs. Men who do not respond to a full dose on two or three different occasions should try other treatments.

Deer velvet is a covering found on the growing bone and cartilage of deer’s antlers. In Eastern medicine, deer velvet is sought after for its Chinese medicinal properties which include boosting one’s endurance and improving one’s immunity. People have also used deer velvet as an aphrodisiac or to treat ED. The randomized double-blind placebo-controlled study on deer velvet by Conaglen et al. (31), no benefit but this study was underpowered involving healthy participants with no sexual dysfunction.
Relaxation of erectile tissue requires nitric oxide from nonadrenergic-noncholinergic neurons and the endothelium.21 Penile tissue from diabetic men with ED demonstrates impaired neurogenic and endothelium-mediated relaxation of smooth muscle,22 increased accumulation of advanced glycation end products (AGEs),23 and upregulation arginase, a competitor with nitric oxide synthase for its substrate L-arginine.24 Normal responses to direct smooth muscle relaxants in most of these studies implies that the impairments are due to decreased synthesis, release, or activity of nitric oxide. The fundamental mechanisms mediating these changes are thought to be the same as for other diabetic complications: increased polyol pathway flux, intracellular accumulation of AGEs, activation of protein kinase C, and increased flux through the hexosamine pathway.25
A component of the increased risk conferred by ED could be testosterone deficiency.24 Low testosterone leads to increased levels of total and LDL cholesterol, as well as to increased production of pro-inflammatory markers and mediators.25 Endothelial dysfunction and increased arterial wall thickness, stiffening, and calcification also ensue. On this basis it has been hypothesized that chronically lowered testosterone may increase CVD risk. Indeed, androgen deficiency has emerged as a predictor of CV events, as well as of all-cause and CV mortality, both in the general population and in patients with CV risk factors, with hypertension, with established CVD, and with ED.26 Viewed from the opposite angle, higher serum testosterone showed a protective role for CV events in elderly men.27 A 2010 meta-analysis limited to studies in middle-aged men found no association between total testosterone (TT) levels and CVD risk.28 However, a more recent meta-analysis involving a larger number of studies identified significant associations between androgen deficiency and increased risk of CVD and CVD mortality.29 It should be stressed, however, that the nature of these studies cannot prove causality. The possibility that low testosterone may be an epiphenomenon, marking poor general health rather than modulating CVD risk per se has to be explored.
Crossref | Google ScholarSee all References Different classes of β-blockers have been postulated to have differential effects on erectile function, with the nonselective β-blockers (eg, propranolol) having more deleterious effects than the more cardioselective medications (eg, atenolol, metoprolol).42x42Weiss, RJ. Effects of antihypertensive agents on sexual function. Am Fam Physician. 1991; 44: 2075–2082
When it comes to boosting sexual performance, many men will walk all over God’s green earth looking for ways to maintain a good sex life. Luckily men, all you have to do is walk — not run — 2 miles a day. This, along with other healthier lifestyle interventions can help obese men reduce their risk of ED, or even “reverse” current impotence, according to a 2005 study. This comes of importance, since maintaining a trim waistline is a good defense for ED, as men with a 42-inch waist are 50 percent more likely to have ED than those with a 32-inch waist. Getting to a healthy weight and maintaining it is a good strategy for preventing and treating ED.
Beta-blockers: A popular blood pressure medication that affects part of the nervous system in an attempt to slow and regulate heartbeats, helping reduce blood pressure. Unfortunately, this same part of the nervous system is also responsible for causing erections, and when beta blockers are used, it indirectly reduces the amount of blood flow to the penis.
 Other treatment options such as penile self-injection therapy, external vacuum pumps and the medicated urethral system for erection are on rare occasions an effective long-term treatment. A very small percentage of men will continue with these treatments as evidenced by a very high drop out rate and a very low refill rate for these treatments. These procedures require extensive planning which interfere with sexual spontaneity and are really not a realistic long-term treatment for young patients with permanent ED. 
Second-generation cardioselective beta-blockers (atenolol, metoprolol, bisoprolol, etc.) can also lead to ED. Atenolol was shown to cause significant reduction of sexual activity compared with placebo in a double-blind, parallel-arm study.22 The same study also showed a significant reduction in testosterone levels with atenolol versus valsartan. An open, prospective study of hypertensive men treated with atenolol, metoprolol and bisoprolol for at least 6 months showed high prevalence of ED – approaching 66 % – in these patients.23
Poor sleep patterns can be a contributing factor for erectile dysfunction, Mucher says. One review published in the journal Brain Research emphasized the intricate relationship between the level of sex hormones like testosterone, sexual function, and sleep, noting that testosterone levels increase with improved sleep, and lower levels are associated with sexual dysfunction. Hormone secretion is controlled by the body’s internal clock, and sleep patterns likely help the body determine when to release certain hormones. 
Diabetes mellitus (DM) is strongly associated with an increased risk of erectile dysfunction (ED), the persistent inability to achieve or maintain an erection sufficient for satisfactory sexual performance, but this condition can be successfully treated in the majority of diabetes patients. ED is present in 32% of type 1 and 46% of type 2 DM patients. Several population- based studies of ED prevalence calculated the odds ratios for the association between ED and various chronic diseases. An odds ratio must be sufficiently greater than 1.0 to identify an increased risk. Diabetes has an odds ratio, ED risk multiplier of 4.1, compared with 1.7 for hyperlipidemia and 1.6 for hypertension. Erectile dysfunction in diabetes mellitus (EDDM) patients has been considered to have an organic etiology. Healthcare providers have long realized that ED can be the first symptom of DM.
Abstract | Full Text PDF | PubMed | Scopus (16) | Google ScholarSee all References These medications cause intracavernosal pressure changes in animal models, and human studies have noted deleterious effects on erectile function, decreased libido, and ejaculatory problems.42x42Weiss, RJ. Effects of antihypertensive agents on sexual function. Am Fam Physician. 1991; 44: 2075–2082
You put your penis in the cylinder and start pumping. The suction creates a vacuum, so blood rushes in to fill the spaces in the spongy tissue of the penis, creating an erection. The erection lasts only as long as the blood stays in, so you slide the band down around the base of your penis, trapping the blood. It's safe to keep the band on for up to 30 minutes.
Diabetes is known to sabotage two body parts that provide essential components of an erection: nerves and blood vessels. Studies suggest that diabetic nerve damage (neuropathy) is the most important risk factor for ED in people with diabetes. If pelvic nerves that trigger penis muscles to relax are impaired, there may be a break in the chain between brain and penis, disrupting erection. Some researchers suspect that an inadequate supply of oxygen to the nerves causes this damage.
The use of shock wave therapy has revolutionized the treatment of many aspects of medicine. High intensity extracorporeal shockwave therapy has been used for the treatment of nephro-urolithiasis while medium intensity shockwave therapy is used by orthopaedic surgeons to treat joint pain as well as tendinitis. Low intensity shockwaves therapy was first noted to improve ischaemia-induced myocardial dysfunction in animal studies when low intensity shockwaves were applied to porcine myocardium (13). Shockwaves induces a localized stress on cell membranes in the same way that shear stress affects endothelial cell membranes (14) and this triggers the release of angiogenic factors, such as increased NO production through increased activity of endothelial NO synthase (eNOS) and neuronal NO synthase (nNOS), platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) (15). These shockwaves also cause membrane hyperpolarization (16), activation of the Ras signaling pathway, non-enzymatic synthesis of NO and induction of stress fibers and intercellular gaps (17).
Crossref | PubMed | Scopus (25) | Google ScholarSee all References In comparison, a randomized placebo-controlled trial of 65 patients given either placebo or 95 mg/d of sustained-release metoprolol for 4 months after percutaneous coronary angioplasty found no significant difference in sexual function between the 2 groups.44x44Franzen, D, Metha, A, Seifert, N, Braun, M, and Hopp, HW. Effects of beta-blockers on sexual performance in men with coronary heart disease: a prospective, randomized and double blinded study. Int J Impot Res. 2001; 13: 348–351

The vacuum device is approved by USA Food and Drug Administration (FDA) for treatment of ED since 1982. Vacuum therapy (VT) works by creating a negative pressure environment around the penis through the use of a cylindrical housing attached to a pump mechanism, which can be manually-operated or battery-operated. Vacuum draws mixed arterial and venous blood into the corporal bodies and distends the corporal sinusoids to create an erected penis. If a pre-loaded constriction band is applied over the base of the penis to prevent outflow of blood and maintain tumescence for intercourse, it is considered a vacuum constriction device (VCD). It is recommended that the constriction band be removed within 30 mins to return the penis to its flaccid state, as prolonged application of the constriction band can compromise both arterial and venous blood flow (7). Some minor side effects associated with VCD are penile discomfort, coldness, numbness, bruising and pain on ejaculation. Major side effects such as penile skin necrosis, gangrene, urethral injury and Peyronie’s disease are very rare (8).

Smoking is an independent risk factor for ED. Tobacco smoking causes direct toxicity to endothelial cells, including decreased eNOS activity, increased adhesion expression and impaired regulation of thrombotic factors.6 A meta-analysis of 19 studies by Tengs and Osgood suggested that 40 % of the impotent men studied were current smokers compared with 28 % who had never smoked.49


For oral erectile dysfunction medicines to work as desired, they must be used properly in the first place. This means taking the medicine 30–45 minutes before engaging in sexual intimacy; taking the drug on an empty stomach or at least avoiding a heavy or high-fat meal before taking the drug (this is especially important when using sildenafil); and engaging in adequate genital stimulation before attempting intercourse. Drinking small amounts of alcohol (one to two drinks) should not compromise the effectiveness of erectile dysfunction medicines, but larger amounts of alcohol can diminish a man’s ability to have an erection.
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