Obesity is a strong predictor of ED as it is associated with other risk factors, such as diabetes, hyperlipidaemia and hypertension.4 Obesity increases the risk of ED by 30–90 % and acts as an independent risk factor for CVD. Obese men with ED have greater impairment in endothelial function than non-obese men with ED.5 Moreover, high BMI causes low testosterone levels, which in turn leads to ED, as observed in a prospective trial involving 7,446 participants.50

A study conducted by Prince Henry’s Institute in Melbourne Australia published in the Medical Journal of Australia found that men over 20 years of age with erectile dysfunction (ED) have twice the risk of cardiovascular incidents than those of men with normal sexual health. It was also found out that 2% of men aged 55 and older experienced major stroke and cardiac arrest after the initial episode of ED, within a year; 11% experienced something within five years.  Experts from Prince Henry’s Institute warned men with these failures to seek advice on erectile dysfunction and high blood pressure. This may indicate a missing vital warning sign of impending heart disease. Why is this happening? Do men with ED predispose themselves to have cardiovascular diseases and strokes or just the other way around?
In a 2005 study, three months of twice-daily sets of kegel exercises combined with biofeedback and advice on lifestyle changes, such as quitting smoking, losing weight, and limiting alcohol, worked far better than just giving the participants advice. “Wearing tight pants will affect impotence along with some other medical conditions like diabetes and heart disease,” which can also affect a man’s degree of impotence, Dr. Jennifer Burns, specializing in family practice with an emphasis on gastrointestinal health at the BienEtre Center, told Medical Daily.
Now that we better appreciate the complex sequence of events necessary for erections to occur, it’s no surprise that testosterone alone yields less than perfect results. Erectile dysfunction represents more than just low testosterone, which is just one facet of the spectrum of dysfunctional phenomena that cause sexual dysfunction. Nonetheless, when testosterone is combined with popular drugs like Viagra®, success is enhanced to an even greater degree—orgasmic function improves, along with erectile capacity and libido.20 Testosterone also activates penile nitric oxide; ultrasound studies have demonstrated a 27% increase in arterial blood flow into the penis with testosterone supplementation.23
Abstract | Full Text PDF | PubMed | Scopus (1528) | Google ScholarSee all References After sexual intercourse, this risk increases approximately 2-fold, to 2 chances per million per hour, but only for the 2 hours after intercourse. For low-risk patients with no history of cardiovascular disease and an annual myocardial infarction risk of 1% per year, the risk increases to 1.01% with weekly sexual activity.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
Diabetes doubles or even triples the chance that you’ll have erectile dysfunction (ED) and that you could develop it a decade earlier than other men. In fact, the two conditions are so closely linked that some experts believe that for men younger than 45, impotence, or ED, could be an early warning sign of diabetes. The good news is that diabetes treatment, especially if you identify type 2 diabetes early, can also ease ED.
Mancia G,  Laurent S,  Agabiti-Rosei E,  Ambrosioni E,  Burnier M,  Caulfield MJ,  Cifkova R,  Clément D,  Coca A,  Dominiczak A,  Erdine S,  Fagard R,  Farsang C,  Grassi G,  Haller H,  Heagerty A,  Kjeldsen SE,  Kiowski W,  Mallion JM,  Manolis A,  Narkiewicz K,  Nilsson P,  Olsen MH,  Rahn KH,  Redon J,  Rodicio J,  Ruilope L,  Schmieder RE,  Struijker-Boudier HA,  van Zwieten PA,  Viigimaa M,  Zanchetti A. European Society of HypertensionReappraisal of European guidelines on hypertension management: a European Society of Hypertension Task Force document, J Hypertens , 2009, vol. 27 (pg. 2121-2158)https://doi.org/10.1097/HJH.0b013e328333146d
Getting blood glucose under control is a good anti-ED tactic. Men with diabetes and poor blood glucose control are two to five times as likely to have ED as those with good control. One study in a group of men who had had type 1 diabetes for up to 15 years with minor complications found that intensive blood glucose control lowered the risk of ED compared with conventional treatment. A study in men with type 2 diabetes found that lowering A1C (average blood glucose in the past two to three months) below 7 percent and reducing blood pressure through a combination of medication, diet, and exercise improved sexual functioning.
Side effects of sildenafil are similar to those from taking niacin or any vasodilator, namely, headaches, lightheadedness, dizziness, and flushing. Some individuals experience a bluish tinge of their cornea, which makes them feel as if they are wearing light blue–tinted sunglasses. This effect can last for several hours. Syncope and myocardial infarction, the most serious side effects, are seen in men who are also taking nitrates for coronary heart disease. Sildenafil also has adverse effects in people with hypertrophic cardiomyopathy because a decrease in preload and after load in the cardiac output can increase the outflow obstruction, culminating in an unstable hemodynamic state.
Following the breakthrough in ED treatment using PDE5-inhibitors, Western medicine has now moved on to a new frontier of regenerative medicine, with stem cell and gene therapy leading the way (25). There is a practical need for novel therapy as a significant portion of diabetic or post-prostatectomy ED patients do not respond to oral pharmacotherapy. To date, stem cells derived from different sites including adipose tissue-derived stem cells, bone marrow mesenchymal stem cells and muscle-derived stem cells have been investigated using animal models for ED, to study their effects on neural, vascular, endothelial or smooth muscle regeneration (25,26).

In subsequent clinical studies, a surprisingly high percentage of EDDM patients–10% to 20%–claimed that the placebo "improved my erections," thus indicating a psychological basis for their ED. In the latter half of the 1980s, objective means were developed that could help determine if a EDDM patient had organic or psychogenic ED. The absence of rigid sleep erections confirmed by penile monitors was one criterion for organic ED. The failure of vasoactive agents (papaverine, Trimix, or prostaglandin E-1 [PGE-1]) injected into the corpora cavernosa to induce penile rigidity was another criterion for organic disease. Intracavernosal maintenance flow rates during pharmacocavernosometry and maximum cavernosal arterial flow during penile Doppler ultrasonography were additional determinants.


"We think that if you have an active sex life it's probably an indicator of a healthy lifestyle, especially in the oldest quartile—those 70 to 80 years old," Andersson said. "From the perspective of a doctor, if a patient asks about erectile dysfunction drugs after a heart attack and has no contraindications for PDE5 inhibitors, based on these results you can feel safe about prescribing it."
Crossref | PubMed | Scopus (23) | Google ScholarSee all References In some elderly men, tadalafil could be detected in the bloodstream 6 days after oral ingestion.74x74Gresser, U and Gleiter, CH. Erectile dysfunction: comparison of efficacy and side effects of the PDE-5 inhibitors sildenafil, vardenafil and tadalafil—review of the literature. Eur J Med Res. 2002; 7: 435–446
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
In particular, patients are classified into three categories (low, intermediate, high) depending on their CV risk profile. Individuals with controlled hypertension belong to the low-risk group where sexual dysfunction can be safely managed with the approved medical therapies regardless of the number or class (with the exception of b-blockers and diuretics) of agents of the patient’s antihypertensive regime. Moreover, patients of this group can safely initiate or reinstitute sexual activity without any need for additional cardiovascular evaluation.

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.
ED is generally associated with significant changes in established cardiovascular risk factors. Atherosclerosis is the main cause of ED development in both the general population and patients with diabetes. However, the prevalence of ED is greater in patients with diabetes than in the general population.8 ED has been shown to occur at rates as high as 50 % in patients with CAD.9 A meta-analysis of 12 prospective cohort studies has provided evidence that ED is a predictor of IHD associated with an increased risk of CVD, stroke and all-cause mortality.10
Crossref | PubMed | Scopus (35) | Google ScholarSee all References Also, if lower blood pressure level was the primary etiology of ED, all classes of antihypertensive agents should be expected to have relatively similar effects on erectile function because of their efficacy in lowering pressure, which has not been seen.6x6Kloner, RA. Erectile dysfunction and cardiovascular risk factors. Hosp Pract (Off Ed). 2001; 36: 41–44 (49-51.)
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
To understand what happens in ED, it's helpful to know some anatomical basics. When aroused by either sensory or mental stimuli, the brain sends a signal through the nerves to the penis, causing the muscles there to relax. This opens up space for blood to flow in and engorge the penis. A membrane within the penis traps blood inside to help maintain the erection, which subsides when the penile muscles contract, forcing blood back into the rest of the body. Any number of things can go wrong in this process, leading to erectile dysfunction.
In the past 6 years, the FDA has approved three oral agents for the treatment of ED: sildenafil, vardenafil, and tadalafil. All three are phosphodiesterase type 5 (PDE-5) inhibitors and work by potentiating the effect of nitric oxide in the penis. In particular, they block the hydrolysis of cyclic guanosine monophosphate to guanosine 5'-monophosphate, thus enhancing nitric oxide–mediated smooth muscle relaxation, increasing blood flow to the penis and facilitating erection.
There are currently two models of the inflatable penile prosthesis (IPP), namely, the two-piece IPP vs. the three-piece IPP. The three-piece IPP consists of a pair of corporal cylinders, a scrotal pump and an abdominal reservoir filled with saline. Owing to the presence of the reservoir, the corporal cylinders can be completely deflated to give the patient the physiological flaccid state when not in use, and likewise a maximally turgid state when inflated (21). The two-piece IPP lacks an abdominal reservoir and is often offered in patients with whom placement of reservoir is challenging or not possible such as following radical cysto-prostatectomy with orthotopic ileal neobladder creation, or patients who had previous open book fracture of the pelvis with metal implants. The concept of ectopic reservoir placement has allowed many of these men the option for three-piece IPP placement (22). Technological advances have improved mechanical reliability, reduced prosthesis infection risk and offered excellent patient and partner satisfaction rate (23).
Your choice of blood pressure medications could make a difference in the bedroom (or wherever you like to have sex). Thiazides (diuretics or “water pills”) and beta blockers are the most likely to cause erectile dysfunction (ED), while alpha blockers the least likely. Alpha blockers work by reducing nerve impulses to blood vessels, allowing blood to pass more easily. Ask your doctor whether these or other blood pressure medications are best for you.
But closer questioning often revealed a very different story—men would admit that struggles to achieve an erection usually preceded a heart attack or other cardiac event by one, two, or three years. Back then, the pattern of erectile dysfunction and cardiac disease was so widespread, that most in the medical profession attributed it to simple “aging,” as common as wrinkles and constipation.
A recent systematic review and meta-analysis of relevant studies in this field confirmed that erectile dysfunction is associated with increased risk of CV events and all-cause mortality[89]. The pooled relative risks were 1.44 (95%CI: 1.27-1.63) for total CV events, 1.19 (95%CI: 0.97-1.46) for CV mortality, 1.62 (95%CI: 1.34-1.96) for myocardial infarction, 1.39 (95%CI: 1.23-1.57) for cerebrovascular events, and 1.25 (95%CI: 1.12-1.39) for all-cause mortality, for men with vs without erectile dysfunction. Of note, the relative risk was higher in intermediate-compared with high- or low-CV-risk populations and with younger age, with obvious clinical implications. Interestingly, the relative risks were higher when erectile dysfunction was diagnosed with the use of a questionnaire compared with a single question (RR = 1.61; 95%CI: 1.38-1.86 vs RR = 1.27; 95%CI: 1.18-1.37, respectively; P = 0.006).
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
Powerful clinical and scientific experience suggests a close link between erectile dysfunction and heart disease. Studies like the Health Professionals Follow-up Study have revealed the risk factors for erectile dysfunction to be very similar to those for heart disease. Hypertension, smoking, diabetes, high cholesterol, obesity, and physical inactivity all strongly predict sexual dysfunction in men, as they do heart disease.1
A variety of personal habits and lifestyle choices have been linked to ED. In some ways, this is a good thing, since habits can be broken and choices reconsidered. What's more, many of the lifestyle factors that contribute to sexual problems are ones that affect overall health and well-being, both physical and mental. Addressing these factors, therefore, can have benefits beyond improving erectile dysfunction.

Crossref | PubMed | Scopus (539) | Google ScholarSee all References After adjusting for age, vascular disease, psychiatric disease, hormonal factors, and marital status, a study of 4462 US Army veterans aged 31 to 49 years found an odds ratio of 1.8 for the risk of developing ED in men who smoked.26x26Mannino, DM, Klevens, RM, and Flanders, WD. Cigarette smoking: an independent risk factor for impotence?. Am J Epidemiol. 1994; 140: 1003–1008
But recently Brandon had some troubles keeping it up. At first, Kayla just thought it was her and that he needed some kind of a change to what they usually did, but later Brandon admitted that as of late, he just couldn’t seem to maintain an erection, and that it took way too much effort to go long. It wasn’t that he wasn’t aroused; his body just wasn’t keeping up.
A substantial body of literature documents the prevalence of ED in men with diabetes. Unfortunately, the majority of these studies do not distinguish between type 1 and type 2 disease, and, therefore, it is difficult to determine if prevalence rates between the two forms of diabetes differ significantly. Acknowledging this limitation in the literature, prevalence estimates of ED in cross-sectional studies of diabetic populations range from 20 to 71% (Table 1). Most of these studies did not control for severity of disease, duration of disease, or control of hyperglycemia.
** Indeterminate risk patients include diabetics, those with mild or moderate stable angina pectoris, past myocardial infarction (2-8 wks) without intervention awaiting exercise electrocardiography, congestive heart failure (NYHA class III), and noncardiac sequelae of atherosclerotic disease (eg, peripheral artery disease and a history of stroke or transient ischemic attack); this patient with ED may require assessment for additional vascular disease using carotid intima-media thickness or ankle-brachial index and subsequent reclassification to low or high risk.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (207) | Google ScholarSee all References Adverse-effect profiles of headaches, flushing, rhinitis, and dyspepsia, without visual changes, mimic those of vardenafil.74x74Gresser, U and Gleiter, CH. Erectile dysfunction: comparison of efficacy and side effects of the PDE-5 inhibitors sildenafil, vardenafil and tadalafil—review of the literature. Eur J Med Res. 2002; 7: 435–446
The initial step in evaluating ED is a thorough sexual history and physical exam. The history can help in distinguishing between the primary and psychogenic causes. It is important to explore the onset, progression, and duration of the problem. If a man gives a history of “no sexual problems until one night,” the problem is most likely related to performance anxiety, disaffection, or an emotional problem. Aside from these causes, only radical prostatectomy or other overt genital tract trauma causes a sudden loss of male sexual function.
The drugs you take to lower your blood pressure may earn you lower marks in the bedroom, by leading to a bout of erectile dysfunction (ED), or the inability to get or maintain an erection during sex. High blood pressure medications such as beta blockers and diuretics do their life-saving job by lessening blood flow to your vital organs—and that includes down under. Less blood flow means no erection. The good news for guys is that not all high blood pressure medication cause ED. Talk with your doctor about switching to the ones that don't.
Phosphodiesterase Inhibitors. The cornerstone of first-line therapy is the PDE-5 inhibitor. No other class of oral agents approaches the efficacy of PDE-5 inhibitors. Yohimbine, trazodone, phentolamine, L-arginine, and OTC herbal remedies have been used with very limited success. The superiority of yohimbine over placebo in the treatment of organic ED is a matter of dispute.9 A recent trazodone study failed to detect any difference between trazodone and placebo on sexual function.10 Oral phentolamine, although available in Mexico, has not been approved by the US FDA for the treatment of ED. Apomorphine, a central dopaminergic receptor drug, has recently been voluntarily withdrawn from FDA consideration for the treatment of ED. The efficacy of ginkgo biloba and Korean red ginseng has yet to be demonstrated by randomized, placebo-controlled trials.
Treatment of ED which was previously confined to invasive procedures, cavernosal injections or to rather ineffective oral medications was revolutionized in 1999 with the introduction of the orally administered PDE5 inhibitor sildenafil. Phosphodiesterase type 5 inhibitors are the first-line therapy for ED of organic aetiology unless there is a specific contraindication to their use. This class of agents is widely used because of its effectiveness and safety.38 Interactions with cardiovascular drugs have been minimal with the exception of nitrates and other nitric oxide (NO) donors (such as nicorandil), where co-administration may result in severe vasodilation and hypotension. However, nitrates are often overused in clinical practice; therefore, the option of their discontinuation should be considered. A strong body of clinical data shows that all three agents (sildenafil, tadalafil, and vardenafil) do not increase the risk of non-fatal myocardial infarction, stroke, or cardiovascular deaths. These drugs do not exacerbate ischaemia or worsen exercise tolerance in patients with known CAD who achieve levels of exercise comparable or greater than that achieved during sexual intercourse.38,39 Phosphodiesterase type 5 is expressed throughout the human body, including the pulmonary and systemic vasculature and hypertrophied myocardium. While currently their only additional indication, beyond ED, is idiopathic pulmonary hypertension (for sildenafil and tadalafil), they show potential to be of benefit in several other conditions, such as CAD and systolic heart failure.39 Mechanisms of benefit of PDE5 inhibitors include pulmonary and systemic vasodilation, increased myocardial contractility, reduced large artery stiffness and wave reflections, improved endothelial function, and reduced apoptosis, fibrosis and hypertrophy through mechanisms involving NO, cyclic guanosine monophosphate, protein kinase G and Rho kinase.39 A very important issue is whether treatment of ED per se (and not of its risk factors and comorbidities) will have an impact on cardiovascular risk. While this applies to all therapeutic modalities of ED, it is particularly pertinent for PDE5 inhibitors, since they represent the mainstay of ED therapy. Data are limited to date. Gazzaruso et al.21 showed a trend of PDE5 inhibitors to reduce cardiovascular morbidity and mortality in diabetic patients with silent CAD and ED, while Frantzen et al.40 showed that 2 years after the introduction of sildenafil, the relative risk of the incidence of CVD among men with ED compared with healthy men significantly decreased from 1.7 to 1.1.
*** High-risk patients include those with unstable or refractory angina pectoris, uncontrolled hypertension, congestive heart failure (NYHA class IV), recent myocardial infarction without intervention (<2 weeks), high-risk arrhythmia (exercise-induced ventricular tachycardia, implanted internal cardioverter defibrillator with frequent shocks, and poorly controlled atrial fibrillation), obstructive hypertrophic cardiomyopathy with severe symptoms, and moderate to severe valve disease, particularly aortic stenosis.

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 (24) | Google ScholarSee all References Erectile function relies on the arterial blood supply from the internal pudendal arteries, which are branches of the hypogastric arterial system (Figure 1). Substantial increases in internal pudendal arterial flow result in pressures within the penis that are comparable to systemic arterial levels.12x12Rampin, O and Giuliano, F. Central control of the cardiovascular and erection systems: possible mechanisms and interactions. Am J Cardiol. 2000; 86: 19F–22F

SOURCES: American Urological Association, "AUA Guideline on the Management of Erectile Dysfunction: Diagnosis and Treatment Recommendations." Barksdale, J. Pharmacotherapy, May 1999; vol 19: pp 573-581. Ferrario, C. Journal of Clinical Hypertension, November/December 2002; vol 4: pp 424-432. Fogari, R. American Journal of Hypertension, January 2001; vol. 14: pp 27-31. Grimm, R. Hypertension, January 1997; vol 29: pp 8-14. Llisteri, J. American Journal of the Medical Sciences, May 2001; vol. 321: pp 336-341. WebMD Medical Reference provided in collaboration with The Cleveland Clinic: "Hypertension: Treatment With ACE Inhibitors."
Yohimbe A number of clinical trials have shown that the primary component of this bark from an African tree can improve sexual dysfunction associated with selective-serotonin reuptake inhibitors (SSRIs) used to treat depression. This herb has been linked to a number of side effects, including increased blood pressure, fast or irregular heartbeat, and anxiety. Yohimbe shouldn't be used without a doctor's supervision.
Another risk factor is that men with type 2 diabetes may produce less than normal amounts of testosterone, a condition called hypogonadism. A 2007 study found that one-third of men with type 2 diabetes had low testosterone levels. Those men were also more likely to have ED, though the link may have to do with weight, not diabetes per se. Being overweight or obese is a risk factor for hypogonadism.
The mechanisms of action by which antihypertensive medications cause ED are currently unknown. Some investigators have theorized that antihypertensive medications affect erectile function by decreasing blood pressure, which reduces the perfusion pressure needed to maintain sufficient blood flow for erections through atherosclerotic penile arteries.37x37Benet, AE and Melman, A. The epidemiology of erectile dysfunction. Urol Clin North Am. 1995; 22: 699–709
Your doctor may also choose to lower your dose of certain medications. Or your provider may switch the type of drug you’re taking if it’s interfering with your sex life. Some medicines used for managing blood pressure, insomnia, anxiety, depression, seizures and prostate problems increase the risk for erectile dysfunction. Beta-blockers (for high blood pressure), SSRIs (often used to treat depression) and the class of drugs called benzodiazepines (like Ativan, Xanax, Librium and Valium) are commonly tied to ED. You may want to speak to your doctor about this.
Erectile dysfunction is common in the CVD patient. It is an important component of the quality of life and it also confers an independent risk for future CV events. The usual 3-year time frame between the onset of ED symptoms and a CV event offers an opportunity for risk mitigation. Thus, sexual function should be incorporated into CVD risk assessment for all men. Algorithms for the management of patient with ED have been proposed according to the risk for sexual activity and future CV events. 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. Testosterone assessment may be useful for both diagnosis of ED, risk stratification and further management. There are issues to be addressed, such as whether PDE5 inhibition reduces CV risk. Management of ED requires a collaborative approach and the role of the cardiologist is pivotal.
Counselling or sex therapy (58% of people find this works for them) –mind-related causes of erectile dysfunction can affect anyone. They are more likely if you experience erectile dysfunction at a younger age. Talking to a counsellor or therapist can help some people overcome erectile dysfunction related to these problems, possibly for good. They can also help you if your erectile dysfunction is causing you stress, as this can make matters worse.
Crossref | PubMed | Scopus (539) | Google ScholarSee all References The MMAS found the total prevalence of minimal to severe ED to be 52% and estimated that more than 617,000 new cases were expected to occur annually in the United States.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
The obvious risks are the same that accompany any surgery: infection, pain, bleeding, and scarring. If for some reason the prosthesis or parts become damaged or dislocated, surgical removal may be necessary. With a general success rate of about 90 percent, any of the devices will restore erections, but they will not affect sexual desire, ejaculation, or orgasm.
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