The use of penile support device such as penile cast worn externally during intercourse has been tried to provide length and rigidity to the penile shaft (24). Each device can be customised to the patient’s penile size and provided an option for patients who are seeking non-pharmaceutical/non-invasive treatment, or have end-organ failure who may not be candidates for, or unable to afford, penile prosthesis implant.
There are no studies specifically assessing the effectiveness of intraurethral suppositories of prostaglandin E1 (PGE-1) in diabetic men. A single randomized clinical trial of the effectiveness of this agent in the general population of men with ED documented that 60% of those who tried this agent were able to achieve successful sexual intercourse.53 Unfortunately, in clinical practice, this agent appears to be considerably less effective.54
PDE-5 inhibitors amplify the intacavernosal production of cGMP in response to nitric oxide. This is achieved through the inhibition of cGMP's breakdown by the enzyme, PDE-5. If the predominant abnormality in the individual EDDM patient is molecular, the higher tissue levels of cGMP will overcome these inhibitory factors and the patient will regain erectile function. If the physical structure (eg, the compliance) of the cavernosal tissue has been significantly compromised by apoptosis of smooth muscle or increased collagen deposits, restoration of erectile function will not be achieved. These structural changes explain the lower efficacy rates of PDE-5 inhibitors in EDDM than in the general population.
Crossref | PubMed | Scopus (539) | Google ScholarSee all References Possible etiologies for ED secondary to hypertension include vascular damage due to hypertensive changes as well as hormonal abnormalities such as elevated prolactin levels.30x30Jaffe, A, Chen, Y, Kisch, ES, Fischel, B, Alon, M, and Stern, N. Erectile dysfunction in hypertensive subjects: assessment of potential determinants. Hypertension. 1996; 28: 859–862
Abstract | Full Text | Full Text PDF | PubMed | Scopus (56) | Google ScholarSee all References However, subsequent studies of older patients who had sexual intercourse in their home and were monitored with ambulatory ECG reported significantly lower heart rates and blood pressure levels.84x84Stein, RA. Cardiovascular response to sexual activity. Am J Cardiol. 2000; 86: 27F–29F
Physical and emotional stress — whether over-exercising, under-sleeping or just dealing with everyday stressors like work and a busy schedule — causes an increase in “stress hormones,” including cortisol and adrenaline. Stress can lower desire for sex. This is because stress can contribute to fatigue or preoccupation with other tasks. It can also significantly affect blood flow by increasing inflammation.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Rates of severe cardiovascular adverse effects were also similar at 1.7 per 1000 person-years of treatment with sildenafil compared with 1.0 events per 1000 personyears with placebo treatment.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
PubMed | Google ScholarSee all References In comparison, a study of 132 patients evaluated by penile duplex ultrasonography after intracorporeal papaverine injection found that hypertension alone was not an independent risk factor for vasculogenic ED.34x34Shabsigh, R, Fishman, IJ, Schum, C, and Dunn, JK. Cigarette smoking and other vascular risk factors in vasculogenic impotence. Urology. 1991; 38: 227–231
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.
Get your diabetes under control. According to Dr. Nehra, the most important number you need to stay on top of is your A1C, which is a blood test that lets you know how well your blood sugar has been controlled for the past few months. Lifestyle changes can help and so can medications. Diabetes medications do not add to your risk for erectile dysfunction, says Nehra.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (46) | Google ScholarSee all References The Princeton Consensus Panel provided guidelines (Table 4) for physicians regarding patients who are being evaluated for their level of risk in resuming sexual activity.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
Crossref | Google ScholarSee all References Other investigators have suggested these medications may exert a hormonal effect. β-Blockers have been associated with decreased free and total testosterone levels in placebo-controlled trials.39x39Rosen, RC and Weiner, DN. Cardiovascular disease and sleep-related erections. J Psychosom Res. 1997; 42: 517–530
These drugs are safe for healthy hearts, but all men with cardiovascular disease should take special precautions, and some cannot use them under any circumstances. The problem is their effect on arteries. All arteries, not just those in the penis, generate nitric oxide, so any artery can widen in response to Viagra, Levitra, or Cialis, causing blood pressure to drop temporarily by 5-8 mmHg, even in healthy men.
Erectile dysfunction (ED) is highly prevalent affecting at least 50 % of men with diabetes mellitus (DM). DM may cause ED through a number of pathophysiological pathways. These include neuropathy, endothelial dysfunction, cavernosal smooth muscle structural/functional changes, and hormonal changes. Lifestyle changes, diabetes control, and treatment of hypogonadism are important as the first step in ED management since there is no curative treatment for ED. Phosphodiesterase type 5 inhibitors (PDE5i) are the first-line treatment option. Intracavernous administration of vasoactive drugs is commonly used as a second-line medical treatment when PDE5i have failed. Alprostadil is the most widely used drug in this second-line setting. The combination of papaverine, phentolamine, and alprostadil represents the most efficacious intracavernous pharmacologic treatment option that may save non-responders to alprostadil. Penile prosthesis implantation can be considered in treatment refractory cases, with excellent functional and safety results in the properly informed patients.
The vascular endothelium has an important role in angiogenesis and vascular repair by producing regulatory substances, including NO, prostaglandin, endothelins, prostacyclin and angiotensin II. These regulatory factors regulate the blood flow to the penis by controlling smooth muscle contractility and subsequent vasoconstriction and vasodilatation. Generally, in erectile tissue, increased blood flow through the cavernosal artery increases shear stress and produces NO, which further relaxes the vascular smooth muscles and increases blood flow in the corpora cavernosa.54 These events cause penile erection. However, in ED, endothelial NO synthesis is reduced and there is increased endothelial cell death (Figure 2).55

Apostolo A,  Vignati C,  Brusoni D,  Cattadori G,  Contini M,  Veglia F,  Magrì D,  Palermo P,  Tedesco C,  Doria E,  Fiorentini C,  Montorsi P,  Agostoni P. Erectile dysfunction in heart failure: correlation with severity, exercise performance, comorbidities, and heart failure treatment, J Sex Med , 2009, vol. 6 (pg. 2795-2805)https://doi.org/10.1111/j.1743-6109.2009.01416.x

Most importantly, herbal supplements are not well regulated in the United States.  Studies have shown that 40-50% of herbal supplements do not even contain the supposed main ingredient, and many contain substances that are not listed which may have dangerous side effects2.  Another study found that over two thirds of the products tested had substituted other plant species for the plants listed on the label, and a third of products also contained other fillers or contaminants3.  A study by the New York State Attorney General of herbal products sold at GNC, Target, Walgreens, and Walmart found that four out of every five products didn’t contain the ingredient they claimed!  Fourteen US states and territories have petitioned Congress to regulate the herbal supplements industry.
WASHINGTON (Mar 09, 2017) - Men who filled prescriptions for erectile dysfunction drugs in the years following a heart attack had a substantially lower risk of dying or being hospitalized for heart failure than men who did not use these drugs, according to a study scheduled for presentation at the American College of Cardiology';s 66th Annual Scientific Session.

Ginkgo biloba. Known primarily as a treatment for cognitive decline, ginkgo has also been used to treat erectile dysfunction -- especially cases caused by the use of certain antidepressant medications. But the evidence isn't very convincing. One 1998 study published in the Journal of Sex & Marital Therapy found that it did work. But a more rigorous study, published in Human Pharmacology in 2002, failed to replicate this finding. "Ginkgo has come out of fashion in the past few years," says Ronald Tamler, MD, assistant professor of medicine and codirector of the men's health program at Mount Sinai Medical Center in New York City. "That's because it doesn't do much. I can say that in my practice, I have not seen ginkgo work -- ever."
Vascular disease: Vascular diseases are those that affect the blood vessels. These diseases include atherosclerosis (hardening of the arteries), hypertension (high blood pressure), and high cholesterol. These diseases, which account for 70% of physical-related causes of ED, restrict blood flow to the heart, the brain, and--in the case of ED--to the penis. Atherosclerosis alone accounts for 50%-60% of ED cases in men over age 60.
If you bike a lot and have a very narrow saddle on your bicycle, consider switching to a "no-nose seat" which is wider at the back than a conventional saddle, allowing more of your weight to be distributed to the sitting bones. Make sure the seat is level or angled slightly downward and at a height that allows your knee to be just slightly bent at the bottom of the pedal cycle. Raising the handlebars on your bike so that you're sitting upright may also help.
As a primary care doctor, my most important job is to tailor treatment for my patients while still making decisions based on the medical literature. So when patients tell me their treatment is causing undesired side effects—like ED—I work with them to create a plan to treat the condition while also finding a way to relieve those side effects. Fortunately, there are ways to deal with medically induced ED.
Whereas management of sexual dysfunction in previously untreated hypertensive patients can be a challenging procedure, confronting the same clinical condition in individuals under antihypertensive regime can be even more demanding. In such cases there will always be a question hovering over physicians head. Is hypertension per se, antihypertensive medication or both, the causative factors provoking sexual dysfunction[15]?
The discovery in 1992 of the second messenger of cavernosal smooth muscle relaxation was the critical step that led to the era of nonhormonal oral drug therapy for ED. In 1998, the multicenter trial of sildenafil in the treatment of ED was published in the New England Journal of Medicine, and the era of the phosphodiesterase type 5 (PDE-5) inhibitor began.1 For 5 years, sildenafil was the primary therapy for men with EDDM. Recently, 2 new PDE-5 inhibitors, vardenafil and tadalafil, were introduced.
Another study showed a forty percent increase of blood flow to the heart within one year of starting a dietary program designed similar to the one described in my book, The End of Heart Disease. Of pertinent note is that, in the same study, the patients following a high-protein Atkins’ diet decreased blood flow to the heart by forty percent in one year.8 These dangerous high-protein diets are a certain path to erectile impotence and a premature cardiac death.
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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