Other effective Diabetic Erectile Dysfunction Treatment therapies available include (a) an intraurethral suppository of the vasodilator drug alprostadil (prostaglandin E1), (b) intracavernosal self injection (penile self injection) of the non-specific PDE drug papaverine, the non-selective alpha-adrenergic antagonist phentolamine, and the vasodilator prostaglandin E1, used alone or in combination, or (c) penile prostheses (penile implants).
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References, 56x56Wallis, RM, Corbin, JD, Francis, SH, and Ellis, P. Tissue distribution of phosphodiesterase families and the effects of sildenafil on tissue cyclic nucleotides, platelet function, and the contractile responses of trabeculae carneae and aortic rings in vitro. Am J Cardiol. 1999; 83: 3C–12C
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
Having your current medication checked – if you are taking medication already, it could be that your erection problems are a side effect. Have a doctor check whether this is the cause of your problems and if it is, you might be able to switch medications and then find that your erectile dysfunction goes away completely – or at least improves. Medications that can cause erection problems include:
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.
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
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References The use of any NO-donor medications should be avoided for 24 hours after the last dose of sildenafil and even longer if there is a suspected prolonged half-life secondary to such conditions as renal insufficiency.10x10Kloner, RA and Zusman, RM. Cardiovascular effects of sildenafil citrate and recommendations for its use. Am J Cardiol. 1999; 84: 11N–17N
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).
Like the case of untreated hypertensive patients, evaluation of sexual dysfunction in hypertensive patients under antihypertensive regime, should primarily exclude other concomitant diseases and pharmaceutical agents. Consecutively, a competent physician with advanced communicational skills should try to “discover” medically induced erectile dysfunction since a vast majority of patients being under complex antihypertensive regimes usually attribute the undesirable effect to normal aging thus not relating it to their current medication. Moreover, even physicians seldom report the cases of sexual dysfunction associated with certain medications. When medically induced sexual dysfunction is finally disclosed and a shift in medication is deemed necessary, b-blockers along with diuretics should generally be the first categories to be changed, unless they are deemed absolutely indicated for the individual patient. Ideally, an ARB could constitute the mainstay of therapy in these cases. If sexual dysfunction still persists, then more effective remedies should be elected paving the way for the introduction of phosphodiesterase-5 inhibitors (PDE-5).
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.
Impotence, also called erectile dysfunction (ED), can be a very frustrating problem. Some men are able to achieve an erection but are not able to maintain one. Others are not able to achieve one at all. Causes of impotence can be both physiological (affecting mostly the body and organs) or psychological (affecting the mind). Luckily, there are natural remedies for impotence you can try.
The choice is yours. You do not have to die of a heart attack, and you do not have to have erectile dysfunction. Both are the result of dietary choices, and you can make a choice right now to protect your life. Do you want to die of a heart attack or don’t you? If you don’t, then are you willing to do what it takes to reduce your risk almost 100 percent? I don’t know about you, but for me, just dropping my risk 20 to 40 percent with medical care is not enough. I want maximum protection.
Luckily, awareness of ED as a significant and common complication of diabetes has increased in recent years, mainly because of increasing knowledge of male sexual function and the rapidly expanding armamentarium of novel treatments being developed for impotence. Studies of ED suggest that its prevalence in men with diabetes ranges from 35–75% versus 26% in general population. The onset of ED also occurs 10–15 years earlier in men with diabetes than it does in sex-matched counterparts without diabetes.
Crossref | PubMed | Scopus (23) | Google ScholarSee all References Only 1 published study has investigated the effect of vardenafil on cardiac function.75x75Thadani, U, Smith, W, Nash, S et al. The effect of vardenafil, a potent and highly selective phosphodiesterase-5 inhibitor for the treatment of erectile dysfunction, on the cardiovascular response to exercise in patients with coronary artery disease. J Am Coll Cardiol. 2002; 40: 2006–2012
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.
Normal penile erection is controlled by two mechanisms: reflex erection and psychogenic erection. Reflex erection occurs by directly touching the shaft of the penis, while psychogenic erection occurs by erotic or emotional stimuli. ED is a condition where erection does not take place by either mechanism. ED can occur because of hormonal imbalance, neural disorders or lack of adequate blood supply to the penis.54 Lack of blood supply can be a result of impaired endothelial function associated with CAD.54
Erectile dysfunction is very common as men age. Erectile dysfunction is frequently a sign of atherosclerosis, a clogging or narrowing of the blood vessels that causes heart attacks. Erectile dysfunction usually comes 3 to 5 years before a heart attack, so after ED is diagnosed, there is time to treat atherosclerosis and prevent a heart attack. Treating atherosclerosis involves diet, exercise, and medications, if necessary. Talk with your doctor about a broken sex life, and you might be able to prevent a broken heart.
There have been some studies to suggest that a placebo effect that improves ED may work for some men. One study found that men taking an oral placebo pill showed as much improvement in ED symptoms as men who took actual medication to improve ED. Conversely, men who were given therapeutic suggestions to improve ED did not see signs of symptom improvement.
Vasculogenic sexual dysfunction is the main cause of sexual dysfunction in untreated hypertensive patients. However, due to the complex etiologic and pathophysiologic nature of sexual dysfunction, exclusion of concomitant diseases and drugs should be the initial step when approaching a hypertensive patient with this clinical condition that is not receiving any antihypertensive medication. Consequently, a significant amount of neurological, psychiatric, urologic and endocrine disorders should be ruled out before vasculogenic sexual dysfunction is diagnosed.
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].
Abnormalities in the vascular, neural, endocrine, muscular, or psychiatric systems can result in ED.2,3 EDDM is due to multisystemic disease. Atrophy or apoptosis of cavernosal smooth muscle can occur due to loss of Bcl-2 expression in cavernosal smooth muscle and lead to ED. Abnormal amounts of advanced glycation end products is a common occurrence. These chemicals may have an effect on potassium channels that facilitate intracellular calcium release and subsequent cavernosal smooth muscle relaxation. Connective tissue synthesis is increased due to transforming growth factor-beta. The decrease in smooth muscle and the increase in collagen decreases the compliance of the erectile tissue. Neuropathic damage to both the somatic and autonomic nerves has been clearly defined in DM. Partial occlusion of the pelvic or intracavernosal arteries, hypogonadotropic hypogonadism, and depression associated with a chronic illness (DM) can all play a primary or secondary role in the development of EDDM. On a molecular level, studies have demonstrated decreased levels of endothelial and neuronal nitric acid synthase (NS) and decreased cavernosal artery and sinusoidal response to nitric oxide. Abnormalities in nitric oxide rapidly render the functional syncytium of the corpora cavernosa unable to synchronously relax. As the patient with diabetes ages, the concentration of constrictors, including endothelin, prostanoids, and possibly angiotensin, increases as the production of the relaxants, including nitric oxide, vasointestinal peptide, and prostacyclin, decreases.
Actually the first simple step to managing your blood pressure is to start tracking it! Get an inexpensive blood pressure cuff at CVS or on Amazon. Download the free Hello Heart app (iOS, Android) from the iTunes Store and Google Play. Start recording your daily blood pressure. Just the simple act of daily recording can have a very beneficial effect.
* Low-risk patients include those with complete revascularization (eg, via coronary artery bypass grafting, stenting, or angioplasty), patients with asymptomatic controlled hypertension, those with mild valvular disease, and patients with left ventricular dysfunction/heart failure (NYHA classes I and II) who achieved 5 metabolic equivalents of the task METS without ischemia on recent exercise testing.
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
A significant proportion (ranging from ∼60 to 90%) of heart failure patients report ED and marked decrease in sexual interest, with ultimately one-quarter reporting cessation of sexual activity altogether.48 Erectile dysfunction contributes further to the poor quality of life and aggravates depression. Of interest, many heart failure patients place a greater importance on improving the quality of life (including sexual activity) than on improving survival. Sexual function correlates with the symptomatic status (i.e. NYHA functional class and 6-minute walk test).48 In the Evaluation of Role of Sexual Dysfunction in the Saarland (EROSS) Program, left ventricular dysfunction was a risk factor for ED independent of heart failure symptoms. While heart failure and ED share common pre-disposing risk factors, heart failure by itself can cause ED or affect engagement to sexual activity. Neurohumoral activation, medication (thiazides), limited exercise capacity, and depression are responsible.49
When antihypertensive medication comes to the fore, certain issues need to be carefully addressed. This is due to the fact that medically induced erectile dysfunction is one of the major reasons for non-adherence and treatment discontinuation, a reality that could have deleterious consequences on patient’s cardiovascular profile and health quality in the long term[38,39].
The views expressed in this article intend to highlight alternative studies and induce conversation. They are the views of the author and do not necessarily represent the views of hims, and are for informational purposes only, even if and to the extent that this article features the advice of physicians and medical practitioners. This article is not, nor is it intended to be, a substitute for professional medical advice, diagnosis, or treatment, and should never be relied upon for specific medical advice.
Intraurethral alprostadil (Muse) provides a less invasive alternative to intrapenile injection. It is a pellet that is inserted 5–10 min before intercourse, and its effects last for 1 h. The response rate is ∼50–60%. It can be used twice daily but is not recommended for use with pregnant partners. Complications of priapism and penile fibrosis are less common than after alprostadil given by penile injection. The cost is ∼$18–24 per treatment.
Most studies into the effect of beta-blockers on ED point to negative effects of first- and second-generation beta-blockers, while beta-blockers with vasodilating effects can improve erectile function. Alpha-blockers, calcium channel blockers, and angiotensin-converting enzyme inhibitors seem to have a neutral effect on erectile function. Multiple previous studies have demonstrated a beneficial effect of angiotensin receptor blockers on erectile function and they should probably be the favoured antihypertensive agents in patients with ED.29
PubMed | Google ScholarSee all References They evaluated 40 patients with coronary artery disease who underwent coronary artery catheterization and whose penile brachial index (PBI) was measured by Doppler ultrasonography. Although a positive correlation was noted between the PBI and the severity of coronary artery obstruction, the relationship was not strong. Also, the degree of PBI abnormality did not effectively stratify the patients according to the severity of their coronary artery blockage. This study concluded that the PBI used alone would not be an effective predictor of ischemic heart disease.
“The presence of erectile dysfunction portends a higher risk of future cardiovascular events, particularly in intermediate-risk men, and may serve as an opportunity for intensification of cardiovascular risk prevention strategies,” wrote Boston University heart specialists Naomi Hamburg, MD and Matt Kluge, MD, in an accompanying editorial. “The findings add to the growing evidence supporting additional trials to determine the clinical impact of erectile dysfunction screening and the appropriate cardiovascular directed evaluation and treatment of men with erectile dysfunction.”
ED is a common complication of diabetes and people with diabetes are also prone to developing cardiovascular complications.48 The risk of ED is relatively high in patients with known CVD. This was supported by a study of men with known CVD, in which ED was substantially predictive of all-cause mortality and the composite of CVD death, admission for heart failure, MI and stroke.17 Macroangiopathy, microangiopathy and endothelial dysfunction are among the mechanisms by which diabetes causes ED.
Erectile dysfunction is common in the patient with cardiovascular disease. It is an important component of the quality of life and it also confers an independent risk for future cardiovascular events. The usual 3-year time period between the onset of erectile dysfunction symptoms and a cardiovascular event offers an opportunity for risk mitigation. Thus, sexual function should be incorporated into cardiovascular disease risk assessment for all men. A comprehensive approach to cardiovascular risk reduction (comprising of both lifestyle changes and pharmacological treatment) improves overall vascular health, including sexual function. Proper sexual counselling improves the quality of life and increases adherence to medication. This review explores the critical connection between erectile dysfunction and cardiovascular disease and evaluates how this relationship may influence clinical practice. Algorithms for the management of patient with erectile dysfunction according to the risk for sexual activity and future cardiovascular events are proposed.
Impotence, or erectile dysfunction (ED), is the inability for a man to sustain an erection long enough for normal, satisfying sexual intercourse. To understand the underlying causes of impotence, it helps to know the basics about how an erection develops, along with potential problems that get in the way. Erections begin in the brain with a thought related to sexual desire. Then a chemical message travels from the brain to the penis. Blood flow to the penis increases as blood vessels leading to the reproductive system relax and allow for increased circulation.
No matter what the cause of erectile dysfunction, it is likely to cause feelings of stress and other emotional reactions. It’s also not uncommon for erection problems to cause tension in a relationship, particularly if one or both partners withdraws emotionally and the problem is not talked about. And it’s possible for a man’s renewed ability to have intercourse after a period of no sexual activity to stir up relationship issues.