After adjusting for cardiovascular risk factors including diabetes, heart failure and stroke, those taking PDE5 inhibitors were found to be markedly less likely to die than those taking alprostadil or no erectile dysfunction drugs. Filling more prescriptions for PDE5 inhibitors appeared to be associated with a greater benefit, although Andersson said that trend should be interpreted with caution because the study was not large enough for a definitive dose-response analysis.
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In fact, one common reason many younger men visit their doctor is to get erectile dysfunction medication. Often, men with erectile dysfunction suffer with diabetes or heart disease, or may be sedentary or obese, but they don’t realize the impact of these health conditions on sexual function. Along with erectile dysfunction treatment, the doctor may recommend managing the illness, being more physically active, or losing weight.
Sexual dysfunction refers to a problem during any phase of the sexual response cycle that prevents the individual or couple from experiencing satisfaction from the sexual activity. The sexual response cycle has four phases: excitement, plateau, orgasm, and resolution. Sexual dysfunction can be caused by physical and emotional factors, or a combination of both. The side effects of some medications also can lead to sexual dysfunction.
The recommended dosage of sildenafil is 50 mg/day, usually taken 1 hour before sexual activity. This dose may be increased to 100 mg or decreased to 25 mg based on side effects.6 PDE5 inhibitors also have a beneficial effect in the treatment of heart failure with reduced ejection fraction as well as pre- and post-capillary pulmonary hypertension. The use of PDE5 inhibitors in the treatment of right heart failure and left ventricular failure associated with combined pre- and post-capillary pulmonary hypertension has been well studied.71,72
First of all, libido (sexual desire) triggers a sympathetic (adrenaline-dependent) nervous system reaction mediated through the thoracic spinal cord. Also important is tactile stimulation, the pleasurable effect of touch, which is mediated through the acetylcholine-dependent parasympathetic nervous system. Both the sympathetic and parasympathetic forces regulate the release of nitric oxide—the universal artery-relaxing agent—from the cells lining the penile arteries and all its smaller branches. Nitric oxide causes the arteries to enlarge, increasing blood flow into the penile tissues. This is followed by compression of blood-draining penile veins, which causes blood to engorge the penis and create an erection.4
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.
PubMed | Google ScholarSee all References In a double-blind, placebo-controlled study, sildenafil was effective in patients with diabetes mellitus.58x58Rendell, MS, Rajfer, J, Wicker, PA, Smith, MD, and Sildenafil Diabetes Study Group. Sildenafil for treatment of erectile dysfunction in men with diabetes: a randomized controlled trial. JAMA. 1999; 281: 421–426
The wide range of prevalence rates noted among the studies can be attributed to a number of factors. First, prevalence rates are affected by the sensitivity and specificity of methods used to assess ED.1 In addition, a number of these studies used medical record review to identify patients with ED, as opposed to anonymous patient reports. It has been shown in other disease states that patients tend to underreport ED when questioned directly by their providers.3 Therefore, the use of validated questionnaires that are either self-administered in an anonymous, neutral setting or administered by an objective third-party interviewer are preferred.
Sexual intercourse is an infrequent cause of myocardial infarction. In a study of 1774 patients after myocardial infarction, only 1.5% of these events occurred within 2 hours of sexual intercourse, and sexual activity was considered a direct contributing factor in 0.9%.8x8Muller, JE, Mittleman, A, Maclure, M, Sherwood, JB, Tofler, GH, and Determinants of Myocardial Infarction Onset Study Investigators. Triggering myocardial infarction by sexual activity: low absolute risk and prevention by regular physical exertion. JAMA. 1996; 275: 1405–1409
Hey folks, It's great to have met you, I really do hope that you enjoyed this article and found it helpful and informative. I Suffered from ED for a few years before taking a short while to reverse it after going down the usual route of those little blue (and expensive) pills, (not an actual cure but a treatment to temporarily relieve the symptoms).Be sure to check out My Highly Recommended products and start taking positive steps in the right direction to cure your erectile dysfunction. And don't forget to grab your free copy of The Testosterone Report and The Morning Wood Report
The truth is medication or psychosexual counselling are the first treatments a doctor will suggest because they’ve been proven to work. If a doctor has approved a medication for you then it’s safe. If you would still like to see if herbal supplements work for you, then there is a list below of supplements thought to work for erectile dysfunction. Just before you invest your money in them, remember they aren’t proven to work:
Penile erection is largely a vascular process, and the penile endothelium and smooth muscle tissue are very sensitive to functional and structural changes. Vasculogenic ED results from an impairment of endothelial dependent or independent smooth muscle relaxation (functional vascular ED, initial stages), occlusion of the cavernosal arteries by atherosclerosis (structural vascular ED, late stages), or a combination of these.3 Current data support a complex interplay between endothelial dysfunction, subclinical inflammation, and androgen deficiency (Figure 1). The relationship between ED and CAD at the clinical level is supported by this common pathophysiological basis. The ‘artery size’ hypothesis explains why patients with CAD frequently report ED before CAD detection.10 According to this hypothesis, for a given atherosclerotic burden, the smaller penile arteries suffer obstruction earlier than the larger coronary arteries (Figure 2). The same concept holds also true in the case of non-obstructing atherosclerosis: since the smaller penile artery have a greater endothelial surface and erection requires a large degree of vasodilation to occur when compared with arteries in other organs, the same degree of endothelial dysfunction will be symptomatic in these smaller vessels but subclinical in the larger ones (i.e. coronaries). In the same context, accelerated arterial ageing (as indicated by increased arterial stiffening that also affects large arteries of ED patients) may be a common background.11,12 Erectile dysfunction is associated with an incremental inflammatory and endothelial-pro-thrombotic activation.13 Interestingly, this activation is equal to that found in CAD patients with no ED, while when these two conditions are combined the burden is additive. Androgen deficiency may be also implicated in the common pathogenetic pathways of ED and CVD; however, this warrants further substantiation.2
It’s crucial that any underlying medical condition, such as angina or diabetes, is detected. So if you’re experiencing problems with ED, book an appointment with your doctor. He or she will assess and examine you to try to establish the cause of the problem, and may refer you for tests. Don’t take any medicine for ED without first discussing it with your doctor.
Despite the existing controversies, available data so far imply the old generation b-blockers (e.g., propranolol) as the major culprits for sexual dysfunction with the newer ones (carvedilol, celiprolol) to exert a less pronounced negative effect[21-24]. A luminous exception to the rule, nebivolol, is a newer agent of its class which significantly ameliorates erectile dysfunction through increased nitric oxide generation, an effect consistently demonstrated in recent studies[25,26]. Diuretics, even on adjunct therapy, constitute another antihypertensive agent negatively associated with sexual function[27-29]. On the other hand, calcium antagonists and angiotensin converting enzyme inhibitors seem to demonstrate a neutral effect[30-32]. Interestingly, angiotensin receptor blockers (ARBs) by blocking the vasoconstrictive action of angiotensin II seem to positively affect erectile function and are thus regarded as a first-line treatment in hypertensive patients with erectile dysfunction[22,25,33-35].
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Diabetes is one of the most common causes of ED. Men who have Diabetes are three times more likely to have Erectile Dysfunction than men who do not have Diabetes. Among men with ED, those with Diabetes are likely to have experienced the problem as much as 10 to 15 years earlier than men without Diabetes. A recent study of a clinic population revealed that 5% of the men with ED also had undiagnosed Diabetes. The risk of ED increases with the number of years you have Diabetes and the severity of your Diabetes. Even though 20% to 75% of men with Diabetes have ED, it can be successfully managed in almost all men.
After analyzing 28 previous studies on the link between ED and heart disease, the researchers found a connection between erectile dysfunction and poor endothelial function. “Blood vessels are unable to fully dilate and allow blood to flow through,” explains Medicalnewstoday.com. “Endothelial dysfunction is an early sign of atherosclerosis, a condition in which plaque builds up in the arteries, raising the risk of heart attack and stroke.” The researchers also determined that there was a thickening of one of the inner two layers of the carotid artery—another heart-disease indicator.
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
Another common reason for failures of oral therapy is the absence of sexual or genital stimulation prior to attempting sexual intercourse. These medicines facilitate an erection by increasing blood flow to the penis, but they do not act as an aphrodisiac or as an initiator of the erection. A man who is not “in the mood” or does not have adequate physical stimulation will not respond with an erection.